Nieuws ziekte van alzheimer


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Gebruik van antidepressiva verhoogt het risico op hoofdletsel onder mensen met de ziekte van Alzheimer

Gebruik van antidepressiva wordt gelinkt met een verhoogd risico op hoofdletsel en traumatisch hersenletsel onder personen met de ziekte van Alzheimer, volgens een nieuwe studie van de University of Eastern Finland. Gebruik van antidepressiva is voorheen gelinkt aan een verhoogd risico op vallen en heupfracturen, maar het risico van hoofdletsel is nog niet eerder bestudeerd. De resultaten zijn gepubliceerd in Alzheimer's Research & Therapy.

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Een eiwit betrokken bij de ziekte van Alzheimer ook betrokken in cognitieve vaardigheden

Van zeldzame mutaties in het amyloÔde precursor eiwit (APP) werd eerder aangetoond dat ze sterk geassocieerd zijn met de ziekte van Alzheimer (AD). Volgens recent onderzoek uitgevoerd aan de Universiteit van Bergen, Noorwegen, kunnen gemeenschappelijke genetische varianten in dit eiwit ook gekoppeld zijn aan intelligentie (IQ) bij kinderen.

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Kunnen omega 3 vetzuren de ziekte van Alzheimer helpen voorkomen?

Volgens een nieuw rapport in Journal of Alzheimer's Disease toont neuroimaging, bij mensen met een hoger omega 3 niveau, een verhoogde bloedstroom in de regio's van de hersenen die instaan voor het geheugen en leren. De incidentie van de ziekte van Alzheimer (AD) zal naar verwachting verdrievoudigen in de komende decennia en er is nog geen genezing gevonden.

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Antipsychotica verhogen kans op sterfte bij Alzheimer

Een recent onderzoek aan de Universiteit van Oost-Finland associeert het gebruik van antipsychotica met een 60 procent verhoogd risico op mortaliteit bij mensen met de ziekte van Alzheimer. Het risico was het hoogst bij het begin van het medicijngebruik en bleef hoog bij langdurig gebruik. Daarenboven toonde het gebruik van twee of meer antipsychotica gelijktijdig een bijna twee keer hoger risico op sterfte dan monotherapie.

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Eiwitten vs neurologische ziektes

De ziekte van Alzheimer (AD), de ziekte van Parkinson (PD) en amyotrofische laterale sclerose (ALS) worden gekenmerkt door samengeklonterde, foutief gevouwen eiwitten en ontsteking in de hersenen. In meer dan 90 procent van de gevallen weten artsen en onderzoekers niet wat de oorzaak is.

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Van Rijn: samen maken we onze samenleving dementievriendelijk

Alzheimer Nederland, PGGM, Deltaplan Dementie en het ministerie van Volksgezondheid, Welzijn en Sport slaan de handen ineen om onze samenleving dementievriendelijker te maken. Vandaag Ė Wereld Alzheimer Dag 2016 Ė start de campagne Samen Dementievriendelijk met de eerste televisiespot. Voor het bevorderen van een dementievriendelijke samenleving (met onder andere een campagne, training en gerichte ondersteuning van beroepsgroepen) heeft staatssecretaris Martin van Rijn (VWS) tot 2020 in totaal 10 miljoen euro uitgetrokken. De campagne die vandaag start, moet er toe bijdragen dat 1 miljoen Nederlanders meer weten over wat leven met dementie betekent en hoe zij mensen met dementie en hun mantelzorgers kunnen helpen.


Antipsychotica verhoogt risico op longontsteking bij Alzheimer

Volgens nieuw onderzoek door de University of Eastern Finland (UEF) worden antipsychotische medicijnen geassocieerd met een verhoogd risico op longontsteking bij mensen met de ziekte van Alzheimer. Aan het begin van de antipsychotische behandeling was het risico op longontsteking het hoogst, en bleef verhoogd bij langdurig gebruik.

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Alzheimer voorkomen door aanpassingen levensstijl - Dr. Greger

Je kunt gerust stellen dat onderzoek naar de ziekte van Alzheimer zich in een "crisissituatie" bevindt. De laatste 20 jaar zijn meer dan 73.000 wetenschappelijke artikelen gepubliceerd, en toch is er weinig klinische vooruitgang geboekt.

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Bosbessen zouden kunnen helpen bij de bestrijding van Alzheimer

De bosbes, al bestempeld als een 'super fruit' omwille van zijn potentieel om het risico op hart- en vaatziekten en kanker te verlagen, kan ook een wapen zijn in de strijd tegen de ziekte van Alzheimer. Nieuw onderzoek uitgevoerd door verschillende teams versterkt dit idee.

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DarmbacteriŽn maken granaatappel metabolieten die kan beschermen tegen de ziekte van Alzheimer

In de zoektocht om gezond te blijven, zijn veel mensen op zoek naar natuurlijke manieren om neurodegeneratieve ziekten te voorkomen. Recente studies tonen aan dat granaatappelextract, dat een rijke bron van ziekte-bestrijdende polyfenolen bevat, kan helpen beschermen tegen de ontwikkeling van de ziekte van Alzheimer.

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Meer risico op krijgen van een beroerte door alzheimer en microbloedingen

PatiŽnten met de ziekte van Alzheimer ťn kleine Ďmicrobloedingení op hun hersenscan hebben een hoger risico op het krijgen van een beroerte. Deze microbloedingen zijn ook een aanwijzing voor een extra ophoping van het alzheimereiwit amyloid in de hersenen. Dit concludeert onderzoeker Marije Benedictus in haar proefschrift waarmee zij op 20 januari promoveert bij VUmc.

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Software kan neurologen helpen bij stellen diagnose alzheimer

Het computerprogramma PredictAD is een nuttig hulpmiddel bij het herkennen van de ziekte van Alzheimer bij mensen met milde cognitieve klachten. Nu moeten neurologen dat doen op basis van klinische gegevens, eventueel aangevuld met MRI-scans en hersenvochtanalyse, maar dat blijkt lastig. Bij aanvullend gebruik van het computerprogramma, blijkt er van elke patiŽnt een voorspelling te kunnen worden gedaan of 'Alzheimerhersenschade' ten grondslag ligt aan de verschijnselen, of niet.

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Ontdekking over synaps misschien aanleiding voor nieuwe behandelingen Alzheimer

Een onderzoeksteam onder leiding van wetenschappers van de UNSW heeft ontdekt hoe de verbindingen tussen hersencellen worden vernietigd in de beginstadia van de ziekte van Alzheimer. Dit werk maakt de weg vrij voor nieuw onderzoek naar mogelijke behandelingen voor deze degeneratieve hersenaandoening.

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Magnesium ionen veelbelovend voor vertraging in progressie Alzheimer bij muizen

Nieuw onderzoek in het FASEB Journal wijst uit dat magnesium ionen de progressie van deze ziekte zouden kunnen vertragen door verstoring van de ontwikkeling van amyloÔde plaques.

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De ziekte van Alzheimer - Overzicht 30 jaar: een nieuw zorgenkind

De ziekte van Alzheimer wordt geassocieerd met de verschijning van karakteristieke neurotoxische proteÔneaggregaten in verschillende hersengebieden. Chemische analyse van deze onoplosbare afzettingen laten zien dat zij bestaan uit een familie van korte eiwitfragmenten, aangeduid als beta-amyloÔde peptiden die zijn afgeleid van een precursor eiwit genaamd APP door de achtereenvolgende werking van twee enzymen.

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Immuunsysteem van de hersenen zou kunnen worden ingezet om de ziekte van Alzheimer te bestrijden

Een nieuwe studie die in het Journal of Neuroinflammation verscheen, suggereert dat het immuunsysteem van de hersenen zou kunnen worden ingezet om de amyloÔde plaques, die een kenmerk zijn van de ziekte van Alzheimer, te helpen op te ruimen.

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Alzheimer-aanleg belemmert ĎGPSí in het brein al bij jongvolwassenen

Alzheimer-patiŽnten lijden aan ernstig geheugenverlies en desoriŽntatie. Een internationaal onderzoeksteam toont nu aan dat een genetisch verhoogd risico voor de ziekte al in jongvolwassenen leidt tot beperking van een hersengebied dat bekend staat als de ĎGPSí van het brein.

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Mensen met dementie zitten gevangen thuis

Mensen met dementie voelen zich vaak gevangen in eigen huis en komen weinig buiten. Dit komt omdat het voor hen steeds lastiger wordt om alleen van A naar B te komen. Ook de mantelzorger raakt zo vaak steeds meer geÔsoleerd. Zo blijkt uit het onderzoek 'Mobiliteit bij dementie', dat op initiatief van PGGM en Alzheimer Nederland is uitgevoerd. Voor dit onderzoek zijn 549 mantelzorgers ondervraagd.

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Miniatuur brein op chip moet meer zicht geven op Alzheimer

Meer zicht krijgen op het ontstaan van de ziekte van Alzheimer door stamcellen te herprogrammeren tot een brein op een chip. Dat is het doel van een Europees onderzoek onder leiding van prof.dr. Cornelia van Duijn van Erasmus MC dat binnenkort van start gaat. Deze chip kan een belangrijke bijdrage leveren aan de vraag wat er misgaat in en rondom de hersenen bij Alzheimer en op welke manier het proces is te stoppen.

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Resveratrol heeft gevolgen voor biomarker van Alzheimer ziekte

Uit de grootste landelijke klinische proef om hoge dosis resveratrol op lange termijn bij mensen met een milde tot matige ziekte van Alzheimer te bestuderen, bleek dat een biomarker die afneemt wanneer de ziekte vordert werd gestabiliseerd bij mensen die de gezuiverde vorm van resveratrol namen.

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Moleculaire structuur van eiwit in Alzheimer plaques kan toxiciteit verklaren

Onderzoekers aan de Universiteit van Illinois in Chicago hebben de moleculaire structuur van ťťn van de eiwitten in de fijne vezels van de bij de ziekte van Alzheimer kenmerkende hersenplaques bepaald. Dit molecuul, amyloÔde beta-42 genaamd, is giftig voor zenuwcellen en wordt beschouwd als de primaire veroorzaker van het ziekteproces.

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Groene thee extract en lichaamsbeweging remmen Alzheimer

Volgens de National Institutes of Health (NIH), treft de ziekte van Alzheimer (AD) minstens 5.500.000 Amerikanen. Wetenschappers zijn momenteel op zoek naar behandelingen en therapieŽn die in gewone voedingsmiddelen te vinden zijn en kunnen helpen de ziekte af te wenden of in zijn geheel te voorkomen. Op het ogenblik hebben Universiteit van Missouri onderzoekers vastgesteld dat een verbinding in groene thee en vrijwillige lichaamsbeweging, ​​de voortgang van de ziekte vertraagt bij muizen en de gevolgen kunnen keren.

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TAU, (een eiwit soort) niet amyloid-beta, triggers neuronale dood in het proces Alzheimer

Nieuw onderzoek wijst tau, geen amyloid-beta (A beta) plaque, aan als de kiem tot aanzet van de neuronen dood in aandoeningen als de ziekte van Alzheimer. Deze vondst, die de heersende theorie dramatisch verandert in de ontwikkelingen van Alzheimer, verklaart ook waarom sommige mensen met plaque opbouw in hun hersenen geen dementie hebben.

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Marihuana bestanddeel zou kunnen helpen bij de behandeling van Alzheimer

Nieuwe preklinische studie geeft aan dat THC de progressie van geheugen ondermijnende ziekte kan vertragen of zelfs stoppen. Extreem lage levels van een bestanddeel in marihuana, bekend als delta-9-tetrahydrocannabinol, of THC, kan de progressie van Alzheimer vertragen of zelfs stoppen, volgens een recente studie door neurowetenschappers van de universiteit van South Florida. Uitkomsten van de experimenten met een cellulair model van Alzheimer werden online vermeld in het Journal of Alzheimer's Disease.

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Lopend onderzoek naar medicijn uit granaatappel tegen de ziekte van Alzheimer en Parkinson

Een onderzoeksteam onder de leiding van Dr Olajide Olumayokun bekijkt de mogelijkheid om derivaten van punicalagin te produceren voor een medicijn dat neuro-ontstekingen zou kunnen behandelen. Het begin van de ziekte van Alzheimer kan worden vertraagd en sommige symptomen afgeremd door een natuurlijke stof gevonden in granaatappel. Ook zou de pijnlijke ontsteking die de ziekten begeleidt, zoals reumatoÔde artritis en de ziekte van Parkinson worden verminderd, afhankelijk van de resultaten van een tweejarig project aan de Universiteit van Huddersfield onder leiding van Dr Olumayokun Olajide, die gespecialiseerd is in de antiontstekingseigenschappen van natuurlijke producten.

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Lichtbehandeling verbetert slaap, depressie en agitatie bij Alzheimer

Een nieuwe studie toont aan dat lichtbehandeling voor het opdrijven van de circadiaanse stimulatie gedurende de dag, de slaap, depressie en agitatie bij mensen met de ziekte van Alzheimer en gerelateerde dementie kunnen verbeteren. Resultaten tonen aan dat de blootstelling aan een lichtbehandeling overdag gedurende vier weken aanzienlijk de kwaliteit van de slaap, de efficiŽntie en de totale slaapduur deed toenemen. Het verminderderde ook significant de scores van depressie en agitatie.

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Onderzoek vindt verhoogde niveaus van DDT metaboliet bij
Alzheimer patiŽnten

Blootstelling aan DDT kan de kans op het ontwikkelen van Alzheimer op latere leeftijd verhogen, aldus een onderzoek door onderzoekers van de UT Southwestern Medical Center.
Hoewel eerdere studies chronische ziekten zoals kanker en diabetes aan DDT gelinkt hebben is dit de eerste klinische studie die deze verboden Amerikaanse pesticide ook aan de ziekte van Alzheimer linkt.

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Een studie uit Penns ontdekt mogelijkheden om de plaques van
Alzheimer te degraderen

Het lichaam is zo gestructureerd om ervoor te zorgen dat alle binnendringende organismen het moeilijk hebben om de hersenen te bereiken, een orgaan uiteraard van cruciaal belang voor de overleving. Bekend als de bloed hersenbarriŤre scheidt het de bloedsomloop af van het buiten de cellen gelegen extracellulaire vocht van de hersenen waardoor het moeilijk is voor minder kleine moleculen uit de bloedbaan binnen te dringen in het centrale zenuwstelsel. Hoewel nuttig belemmert deze blokkade ook de werking van geneesmiddelen voor neurologische aandoeningen zoals Alzheimer .

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Alzheimer en vasculaire veranderingen in de nek.

Buffalo, NY - Studies over de ziekte van Alzheimer en andere vormen van dementie hebben zich lang gericht op wat er gebeurt in de hersenen. Nu rapporteert een internationaal onderzoeksteam dat Alzheimer en "mild cognitive impairment" bestudeert, significante bevindingen van vasculaire afwijkingen buiten de hersenen. Deze resultaten zijn belangrijk voor een beter begrip van Alzheimer en andere neurologische aandoeningen geassocieerd met veroudering.

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Kunnen bepaalde kruiden de ziekte van Alzheimer afwenden?

SLU dieronderzoek suggereert dat antioxidant extracten van groene munt en rozemarijn het leren en het geheugen verbeteren.

ST. LOUIS ó Verbeterde extracten gemaakt van speciale antioxidanten in groene munt en rozemarijn verbeteren het leren en het geheugen, een onderzoek dat gedaan is met een diermodel aan de Saint Louis University.

ĒWij vonden dat deze gepatenteerde verbindingen tekorten verminderen die veroorzaakt worden door milde cognitieve stoornissen, die een voorloper kunnen zijn van de ziekte van Alzheimer,Ē zei Susan Farr, Ph.D, research professor geriatrie van de Saint Louis University School of Medicine.

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Koper oorzaak van Alzheimer

Koper blijkt ťťn van de belangrijkste ecologische factoren te zijn dat het begin en de progressie activeert van de ziekte van Alzheimer door het verhinderen van de tegenwerking van de accumulatie van toxische eiwitten in de hersenen. Dat is de conclusie van een studie die in het tijdschrift Proceedings van de National Academy of Sciences verscheen.

"Het is duidelijk dat na verloop van tijd het cumulatief effect van koper het systeem dwarsboomt waarmee amyloÔde beta wordt verwijderd uit de hersenen," zei Rashid Deane, Ph.D., professor onderzoeker aan de University of Rochester Medical Center (URMC) Afdeling Neurochirurgie, lid van het Center for Translational Neuromedicine en hoofdauteur van de studie. "Deze stoornis is ťťn van de belangrijkste factoren die ervoor zorgen dat eiwit kan cumuleren in de hersenen en plaques vormen die kenmerkend zijn voor de ziekte van Alzheimer."

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Nieuwe inzichten in de tegenspraak dat het veelbelovende medicijn voor Alzheimer (Bexarotene) niet op patiŽnten getest moet worden

Ongeveer een jaar geleden, publiceerde het toonaangevende tijdschrift ĎScienceí een
artikel over Bexarotene als mogelijk geneesmiddel voor Alzheimer. Een significante
doorbraak en een belangrijk uitgangspunt voor verder Alzheimer onderzoek.
De onderzoeksgroep van Bart De Strooper Ė Alzheimer onderzoeker bij VIB en KU Leuven Ė heeft dit medicijn in samenwerking met de groep van Rudi D'Hooge - KU Leuven - en wetenschappers van Janssen Pharmaceutica ( Beerse ), ook in diverse Alzheimer-dierproefmodellen getest.

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Uitleggen hoe extra vergine olijfolie beschermt tegen de ziekte van Alzheimer

Het mysterie van hoe precies de consumptie van olijfolie extra vierge helpt het risico van de ziekte van Alzheimer (AD) te verminderen, kan liggen in een onderdeel van de olijfolie, dat helpt de abnormale AD eiwitten uit de hersenen te pendelen, rapporteren wetenschappers in een nieuwe studie. Het wordt weergegeven in het dagboek ACS chemische Neuroscience. Amal Kaddoumi en collegaís merken op dat AD ongeveer 30 miljoen mensen wereldwijd treft, maar in de mediterrane landen de overheersing lager is. Wetenschappers hebben dit een keer toegeschreven aan de hoge concentratie van de gezonde enkelvoudig onverzadigde vetten in olijfolie ó geconsumeerd in grote hoeveelheden in het mediterrane dieet. Recenter onderzoek veronderstelde dat het werkelijke beschermende middel, een stof genaamd oleocanthal zou kunnen zijn, het effect heeft zenuwcellen te beschermen tegen het soort schade dat zich voordoet in AD. Kaddoumiís team zochten bewijs of oleocanthal helpt om de accumulatie van bŤta-amyloid (Aβ) in de hersenen te verminderen, de vermoedelijk de boosdoener in AD.

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Extracten van groene thee en rode wijn verstoren het Alzheimer traject in hersencellen

De natuurlijke chemische stof, gevonden in groene thee en rode wijn, kan een belangrijke stap, bij het traject naar de ziekte van Alzheimer, verstoren. Aldus nieuw onderzoek van de Universiteit van Leeds. Reeds in een eerder laboratoriumexperiment stelden de onderzoekers vast dat het proces waarmee schadelijke eiwitten zich met bosjes aan hersencellen vastklampen, veroorzaakte dat ze afstierven. Ze waren in staat om dit traject met behulp van de gezuiverde uittreksels van EGCG uit groene thee en resveratrol * van rode wijn te onderbreken. Resveratrol is een polyfenol dat in diverse plantensoorten voorkomt, maar vooral in de schil van blauwe druiven. De bevindingen, gepubliceerd in The Journal of Biological Chemistry, bieden potentiŽle nieuwe doelstellingen voor de ontwikkeling van geneesmiddelen voor de behandeling van de ziekte van Alzheimer, die ongeveer 800.000 mensen in het Verenigd Koninkrijk alleen al treft, en waarvoor helaas momenteel nog geen remedie bestaat.

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Melatonine en bewegen helpen tegen Alzheimer bij muizen

Verschillende anti-aging behandelingen werken samen en verlengen het leven met jaren. De combinatie van twee neuroprotectieve therapieŽn, vrijwillige lichaamsbeweging en een dagelijkse inname van melatonine hebben aangetoond een synergetisch effect te hebben op verslechtering van de hersenen bij knaagdieren met drie verschillende mutaties van de ziekte van Alzheimer.  Een studie, uitgevoerd door een groep onderzoekers van het Barcelona Biomedical Research Institute (IIBB) in samenwerking met de University of Granada en de Autonomous University of Barcelona, toont het gecombineerde effect van neuroprotectieve therapieŽn tegen de ziekte van Alzheimer bij muizen.

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Wetenschappers keren Alzheimer-achtig geheugenverlies in dieren modellen om door het blokkeren van EGFR signaaltransductie

EGFR-remmers, die gebruikt worden om kanker te bestrijden, tonen een verrassende werkzaamheid bij vliegen- en muizenmodellen en beta amyloid-geassocieerd geheugenverlies. Cold Spring Harbor, NY - Een team van neurowetenschappers en chemici van de VS en China publiceren vandaag een onderzoek waaruit blijkt dat een categorie van momenteel gebruikte anti-kanker medicijnen evenals verscheidene eerder geteste synthetische verbindingen effectiviteit laten zien in het omkeren van geheugenverlies bij twee dierenmodellen met Alzheimer.

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Enzym in de hersenen extra desastreus voor de ziekte van Alzheimer

Onderzoekers aan de Sanford-Burnham universiteit ontdekken dat het enzym dat toxische hersenplaques veroorzaakt bij de ziekte van Alzheimer ook geheugen- en cognitieve functies beschadigt via een ander mechanisme. De onderligggende oorzakn van de ziekte van Alzheimer worden niet geheel begrepen, maar er is duidelijk bewijs dat een ophoping van beta-amyloid die wordt veroorzaakt door verschillende enzymen, waaronder het zo genaamde BACE1, een rol speelt. De meeste Alzheimer patiŽnten hebben verhoogde spiegels van BACE1, dat op zijn beurt zorgt voor meer beta-amyloid eiwit dat schadelijk is voor de hersenen.

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Mayo Clinic researchers identificeren een nieuw enzym ter bestrijding van de ziekte van Alzheimer

Een enzym dat een krachtig nieuw werktuig zou kunnen zijn ter bestrijding van de ziekte van Alzheimer is ontdekt door onderzoekers in Mayo Clinic in Florida. Het enzym ó bekend als BACE2 ó vernietigt bŤta-amyloÔde, een fragment van het giftige proteÔne dat de hersenen in de war brengt van patiŽnten die de ziekte hebben. De bevindingen werden online gepubliceerd in de Science Journal Moleculaire Neurodegeneratie. De ziekte van Alzheimer is de meest voorkomende aandoening van het geheugen. Het treft meer dan 5,5 miljoen mensen in de Verenigde Staten. Ondanks dat de aandoening een enorme financiŽle en persoonlijke tol eist, is een doeltreffende behandeling nog steeds niet gevonden.

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Chronische ontsteking in de hersenen leidt tot de ziekte van Alzheimer

Onderzoek dat vandaag wordt gepubliceerd in het open access tijdschrift BioMed Centralís open access journal ďJournal of NeuroinflammationĒ suggereert dat chronische ontsteking een predispositie kan zijn voor de hersenen om de ziekte van Alzheimer te ontwikkelen. Tot nu toe was het moeilijk de rol van ontsteking bij de ziekte van Alzheimer vast te stellen, vooral omdat trials met NSAIDís conflicterende resultaten leek te geven. Hoewel de ADAPT (afkorting voor de ziekte van alzheimer anti-inflammatoire preventie trial) vroegtijdig gestopt werd suggereren recente resultaten dat NSAIDís mensen met vroege stadia van Alzheimer kunnen helpen maar dat een langdurige behandeling nodig is om voordeel te zien.

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Relatie tussen ingrediŽnt smaakstof voor margarine en sleutel tot ziekteproces van Alzheimer

Een nieuw onderzoek geeft aanleiding tot bezorgdheid over de voortdurende blootstelling van werknemers in de industrie aan een voedings ingrediŽnt smaakstof die wordt gebruikt voor de productie van het kenmerkende boterachtige aroma en het aroma van magnetron popcorn, margarines, snacks, snoep, gebakken goederen, pet levensmiddelen en andere producten. Er is bewijs gevonden dat het ingrediŽnt, Butaandion (DA), de schadelijke effecten van een abnormaal herseneiwit intensiveert gekoppeld aan de ziekte van Alzheimer. De studie verschijnt in het ACS tijdschrift Chemical Research in de toxicologie.

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Onderzoekers laten zien hoe bij de ziekte van Alzheimer plaques leiden tot verlies van stikstof in de hersenen

Een onderzoeker aan de universiteit van Pittsburg School of Medicine, heeft in samenwerking met wetenschappers van het National Institutes of health (NIH) ontdekt dat de dodelijke plaques bij de ziekte van Alzheimer een relatie aangaan met bepaalde cellulaire eiwitten om de normale signalen die de bloedtoevoer naar de hersenen handhaven te remmen. Hun bevindingen, die kunnen leiden tot nieuwe benaderingen van behandelen van dementie, zijn onlangs gepubliceerd in Public Library of Science One.Niveaus van stikstof (NO)- een signalerings-molecuul dat helpt de bloedstroom te regelen, het immuumsysteem en neurologische processen staan bekend laag te zijn in de hersenen van mensen die de ziekte van Alzheimer hebben, maar de reden voor dat is niet duidelijk, zegt co-auteur Jeffrey S. Isenberg, MD, MPH universitair hoofddocent, afdeling long-, Allergie, en Critical Care Medicine, Pitt School of Medicine.

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Voorkom Alzheimer met de kleur paars

Als je paarse vruchten eet zoals bramen en als je groene thee drinkt kunnen ziektes voorkomen worden met inbegrip van Alzheimer, MS en Parkinson's zo claimt een universiteit uit Manchester. Baanbrekend onderzoek door professor Douglas Kell gepubliceerd in het blad "Archives of Toxiocology" heeft opgeleverd dat het belangrijkste deel van de meest voorkomende ziektes gedeeltelijk veroorzaakt wordt door slecht opgenomen ijzer dat een produktie start van gevaarlijke gifstoffen die een reactie kunnen geven bij levende organismen. Deze gifstoffen "hydroxil" radicalen genoemd ontaarden in verschillende soorten ziektes in verschillende gedeeltes van het lichaam. Om het lichaam te beschermen tegen deze gevarieerd gevaarlijk slechte ijzer opnames is het heel belangrijk voedingsstoffen te nemen die bekend staan onder ijzer bindings componenten, die het ijzer effectief kunnen binden. Vruchten en groenten met heldere kleuren zijn uitstekende bronnen van ijzerbinding, zoals ook groene thee en paarse vruchten worden beschouwd als de beste produkten die ijzer kunnen binden.

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Jack


Mankementen aan de bloedvaten die in verband staan met hartziekte hebben ook een link met Alzheimer

Een mankement aan de vaatwand van bloedvaten dat een verband heeft met hartziektes blijkt ook een rol te kunnen spelen in de ontwikkeling van Alzheimer blijkt uit een studie gepubliceerd in "circulation research" blad van de Amerikaanse hart organisatie. De ziekte van Alzheimer is een progressieve aandoening van de hersenen, die mensen beinvloedt van 60 jaar en ouder, die hen berooft van hun geheugen, redenatie en andere cognitieve vaardigheden.Vijf miljoen Amerikanen hebben Alzheimer volgens het nationaal instituut van de gezondheid.

Twee duidelijk te onderscheiden bijzonderheden in het brein zijn signalen van Alzheimer.Neuronen complicaties,fiber dat voornamelijk bestaat uit een proteine dat "tau" wordt genoemd en dat voor komt in zenuwcellen. Of neuronen en plaques van "Amyloid" een verzameling tussen neuronen van proteine fragmenten genaamd "Amyloid" beta peptides.

Eerder onderzoek heeft aangetoond, dat mensen met meervoudige risico's m.b.t. hart- en vaatziekte ook een verhoogd risico hebben voor de ziekte van Alzheimer. Het belangrijkste onderdeel voor deze hart- vaatziekte risico's is een nitraat oxyde afwijking in het "Endothelium" de laag van cellen in de vaatwand van de bloedvaten.Nitraat oxyde is het belangrijkste m.b.t. verwijding van de bloedvaten, het stromen van het bloed en het brengen van zuurstof en voedingsstoffen naar het omliggende weefsel

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Makozie


Studies geven al in een zeer vroeg stadium hersen veranderingen aan die samenhangen met het genetische risico op de ziekte van Alzheimer

Dit kan inhouden, dat preventieve therapieen worden ontwikkeld. Wat zijn de vroegste hersenveranderingen die in verband staan met de ontwikkeling van de ziekte van Alzheimer? Een wetenschappelijk verslag gepubliceerd in het oktober nummer van het blad "de ziekte van Alzheimer" ontdekt verminderde activiteit van het energie opwekkende enzym in de hersenen van overleden jong volwassen hersen donoren die een algemeen genetisch risicofactor hebben voor de ziekte van Alzheimer. Dit voorafgaand aan de proteine veranderingen en microscopische afwijkingen gewoonlijk in verband gebracht met de ziekte en bijna vijf decennia voor de leeftijd waarbij ze misschien geheugen en denkmoeilijkheden zouden kunnen ontwikkelen.

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Vertaling: Makozie


Relatie tussen vitamine D-tekort en leerstoornis bij Alzheimer

Een nieuw onderzoek, gepubliceerd in de International Journal of Neuroscience, suggereert dat een vitamine D-tekort bij personen die de ziekte van Alzheimer hebben het onvermogen om te leren verergert. Alzheimer is de meest voorkomende vorm van dementie.

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Annelies


TV - Holland Doc: Mam

Theatermaakster Adelheid Roosen filmde haar dementerende moeder samen met de mensen die het dichtst bij haar staan. Ze maakte van de beelden een intiem portret.

Link


Hersenbeschermingsenzyme zou Alzheimer bestrijden

Herstelniveaus van een zenuwbeschermend enzyme biedt een nieuwe aanpak om geneeswijzen tegen Alzheimer te ontwikkelen, zeggen US onderzoekers.

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Pieter Tau


Bij diegene die leiden aan vroege dementie kan de carriŤrekeuze bepalen waar de ziekte in de hersenen ontstaat

Bij een internationale onderzoek van patiŽnten met een verwoestende vorm van dementie, die vaak bij middelbare leeftijd toeslaat, hebben onderzoekers fascinerende bewijzen gevonden dat de loopbaan invloed kan hebben waar de ziekte in de hersenen aangrijpt. De studie werd geleidt door Baycrest's Rotman Research Institute in samenwerking met het Memory and Aging Centre van de Universiteit van CaliforniŽ, San Francisco en een aantal Amerikaanse en Europese medische centra. Het verschijnt vandaag on-line op de Article in Press section van het nieuwsbulletin Neuropsychologia, voordat het gepubliceerd wordt.

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Wouter


Acetylering draagt mogelijk bij aan dementie en de ziekte van Alzheimer

(Acetylering is een acylering met azijnzuur. Dit is een scheikundige reactie waarbij een molecuul aan een vetzuur wordt gekoppeld.)

Een nieuwe studie onthult een eiwitmodificatie die kan bijdragen tot de vorming van zenuw beschadigende verbindingen in de menselijke hersenen. Het onderzoek, gepubliceerd door Cell Press in het tijdschrift Neuron op 23 september 2010 kan leiden tot nieuwe strategieŽn voor de behandeling van degeneratieve zenuw ziekten die het gevolg zijn van ziekmakende samenvoeging met het tau-eiwit.

Tau-eiwit is normaal aanwezig in het centrale zenuwstelsel waar het bijdraagt aan het verstevigen van de zenuwcellen; de micro tubuli (buisjes in de nieren) die het neurale cyto skelet (een cyto skelet is een netwerk van vezels in een cel dat de onderdelen op hun plaats houdt) vormen worden verstevigd. Veranderingen in het Tau-eiwit worden toegeschreven aan dementie en de ziekte van Alzheimer. "Degeneratie van de zenuwen wordt toegeschreven aan de opeenstapeling van fosforilering van het tau-eiwit (p-tau). Echter, de moleculaire mechanismen die ten grondslag liggen aan deze abnormale opstapeling van tau is niet verklaard.

"We weten dat een enzym genaamd SIRT1 verminderd aanwezig is in de hersenen van Alzheimer patiŽnten en dat deze vermindering verband houdt met de opeenstapeling van p-tau. Bij een proef met muizen met de ziekte van Alzheimer blijkt dat een overmatige aanwezigheid van het enzym SIRT1 beschermt tegen zenuw verlies", aldus senior auteur van deze studie, Dr . Li Gan van het Gladstone Instituut voor Zenuwziekten in San Francisco, CaliforniŽ. "Maar hoe SIRT1 beschermt tegen tau-bemiddelende degeneratie van het zenuwweefsel is niet duidelijk."

SIRT1 is een ont-acetylase, een enzym dat acetylgroepen van eiwitten verwijdert. Net als fosforilering, regelt acetilering veel verschillende cellulaire functies, met inbegrip van cyto skelet dynamiek. "Om te bepalen of tau wordt geacetyleerd en of tau acetylering bijdraagt aan tau opeenstapeling, onderzoeken we tau acetylering in de zenuwen, proeven met muizen of tauopathie (ouderdom gerelateerde ziekten), en onderzoeken we ook de hersenen van mensen met Alzheimer," zegt Dr Gan.

Dr Gan groep vond dat tau acetylering de afbraak van p-tau voorkomt. PatiŽnten in een vroeg of een gemiddeld stadium van ouderdoms gerelateerde ziekten (tauopathie) vertonen een verhoogde tau acetylering. De onderzoekers gingen verder en tonen aan dat het hebben van SIRT1 een verhoogde waarde geeft van geacetyleerd en ziekmakend tau, terwijl een kleine molecule remmer (stof die de werking van een enzym, hormoon of geneesmiddel afneemt) van P300, een enzym waarvan bekend is dat het acetyl groepen hecht aan eiwitten en de tau ont-acetylering bevorderd en de p-tau associatie met ziekmakende omstandigheden uitschakelt.

Hoewel het verband tussen tau acetilering en tau fosforilering onbekend is geven de resultaten nieuw inzicht in tau-bemiddelende kennis van zenuwziekten (neuropathologie).

"Onze bevindingen ondersteunen het model dat de abnormaal verhoogde acetylering in een vroeg stadium van de ziekte de zuivering van p-tau van neuronen kan blokkeren en leidt tot een opeenstapeling", concludeert Dr Gan. "Onze observatie dat p300 bijdraagt aan een verminderde tau acetylering en effectief p-tau verwijderd, bevordert het idee dat het tussen beide komen met tau acetylering een nieuwe aanpak kan zijn voor het verminderen van tau-gerelateerde pathologie."

De onderzoekers zijn: Sang-Won Min, Gladstone Institute, University of California, San Francisco, CA, University of California, San Francisco, CA; Seo-Hyun Cho, Gladstone Institute, University of California, San Francisco, CA, University of California, San Francisco, CA; Yungui Zhou, Gladstone Institute, University of California, San Francisco, CA; Sebastian Schroeder, Gladstone Institute, University of California, San Francisco, CA, University of California, San Francisco, CA; Vahram Haroutunian, The Mount Sinai School of Medicine, New York, NY; William W. Seeley, University of California, San Francisco, CA; Eric J. Huang, University of California, San Francisco, CA; Yong Shen, Haldeman Laboratory of Molecular and Cellular Neurobiology, Sun Health Research Institute, Sun City, AZ; Eliezer Masliah, University of California at San Diego, La Jolla, CA; Chandrani Mukherjee, Johns Hopkins University, School of Medicine, Baltimore, MD; David Meyers, Johns Hopkins University, School of Medicine, Baltimore, MD; Philip A. Cole, Johns Hopkins University, School of Medicine, Baltimore, MD; Melanie Ott, Gladstone Institute, University of California, San Francisco, CA, University of California, San Francisco, CA; and Li Gan, Gladstone Institute, University of California, San Francisco, CA, University of California, San Francisco, CA.

Contact: Cathleen Genova
cgenova@cell.com
Tel.: 001-617-397-2802 001-617-397-2802
Cell Press

Vertaald door Pauline Laumans
Bron


Onderzoekers van Gladstone hebben een nieuwe strategie ontwikkeld om giftige eiwitten te verminderen die verband houden met de ziekte van Alzheimer.

Tau acetylatie kan bijdragen aan de ziekte van Alzheimer en andere vormen van dementia.

Wetenschappers van het Gladstone Instituut voor zenuwziekten (GIND) hebben nieuwe behandelmethode ontwikkeld om de giftige eiwitten te verminderen met betrekking tot de ziekte van Alzheimer en andere zenuw degenererende ziekten. De resultaten kunnen leiden tot nieuwe behandelmethodes voor deze ziekten. "We hebben het eiwit tau onderzocht dat sterk betrokken is bij de ziekte van Alzheimer," zegt Li Gan, PhD, senior auteur van deze onderzoeksstudie. "Tau vormt giftige eiwitten samenklonteringen in de hersenen van patiŽnten met de ziekte van Alzheimer."

Tau is een algemeen aanwezig eiwit in het centraal zenuwstelsel waar het bijdraagt aan het stabiliseren van het cyto skelet (een cyto skelet is een netwerk van vezels in een cel dat de onderdelen op hun plaats houdt) dat de zenuwverbindingen bevordert. Veranderingen in tau veroorzaken degeneratie van de zenuwen in de menselijke hersenen, en veranderingen aan tau door de toevoeging van fosfaten groepen (p-tau) vormt opeenhopingen en beschadigd de zenuwen. StrategieŽn om p-tau van zenuwen te verwijderen zijn hard nodig. "We weten dat niveaus van het enzym SIRT1 verlaagd zijn in de hersenen van Alzheimer patiŽnten en deze daling houdt verband met het aantal van tau7 opeenhopingen. We weten ook dat SIRT1 beschermt - in een proef tegen zenuw degeneratie met muizen," zegt Dr. Gan. "Maar we wisten niet hoe dit alles verband houdt met elkaar."

Een belangrijke ontdekking is dat SIRT1 een ont-acetylase is, een enzym dat de acetylgroepen verwijdert van eiwitten. Zoals fosforilatie reguleert acetylatie veel verschillende celfuncties. (Acetylatie betekent het binden van een acetylgroep aan een vreemde stof in het lichaam) "Daarom willen we weten of tau is geacetyleerd" zegt Dr. Gan.

In deze studie die op 23 september 2010 is gepubliceerd in het tijdschrift "Neuron" rapporteert de onderzoeksgroep van Dr. Gan's dat feitelijk tau geacetyleerd is. Verder rapporteren ze dat patiŽnten in een begin stadium of gemiddeld stadium van de ziekte van Alzheimer een verhoogd niveau vertonen van tau acetylatie.

De onderzoekers tonen aan dat het hebben van SIRT1 verhoogde niveaus van zowel geacetyleerde tau als van p-tau in zenuwen laat groeien in kweekschalen. Het onderzoeksteam vroeg zich af of het hebben van de productie van geacetyleerd tau een effect heeft. Belangrijker is, wanneer zij P300 hadden, een enzym waarvan bekend is dat het acetyl groepen voegt aan eiwitten, de neuronen minder geacetyleerd tau en giftig p-tau hadden.

Het onderzoek toont aan dat het ophelderen van giftig p-tau wordt geblokkeerd door acetylatie. "De abnormaal hoge niveaus van acetylatie in het beginstadium van de zeikte kunnen leiden tot het vormen van giftige eiwitten opeenhopingen bij mensen met de ziekte van Alzheimer en andere degeneratieve zenuwziekten" legt Dr. Gan uit.

"De studie suggereert dat tussen beide komen met de tau acetylatie een nieuwe benadering kan zijn om tau gerelateerde ziekten te verminderen," zegt Dr. Mucke, directeur van het Gladstone Instituut voor Zenuwziekten. "In feite hebben Dr. Gan en haar team reeds een aantal kleine moleculen samenstellingen geÔdentificeerd die giftig p-tau verwijderen in zenuwen. Dit kan een nieuw klasse van anti Alzheimer medicatie vertegenwoordigen." Het onderzoeksteam omvat Gladstone's San-Won Min, Seo-Hyun Cho, Yungui Zhou, Sebastian Schroeder and Melanie Ott; UCSF's William Seeley and Eric Huang; Vahram Haroutunian of Mt. Sinai School of Medicine; Chandran Mukherjee, David Meyers and Philip Cole of Johns Hopkins; Yong Shen of Haldeman Laboratory; and Eliezer Masliah of UC San Diego. Het onderzoek werd mogelijk gemaakt door: the Whittier Foundation, S.D. Bechtel Jr. Foundation, NIH, en FAMRI.

Li Gan's primaire betrekking met het Gladstone Instituut voor zenuwziekten is dat ze assistent onderzoeker is en waar haar loboratorium is en ze haar onderzoek uitvoert. Ze is ook assistent professor in de Neurologie aan het UCSF. Gladstone Instituut is een niet voor winst, onafhankelijk onderzoeks - en scholing instituut, bestaande uit het Gladstone Instituut voor Hart- en vaatziekten, het Gladstone Instituut voor Virologie en Immunologie en het Gladstone Instituut voor of Zenuwziekten. Een onafhankelijk bestuur, financiŽn en onderzoekprogramma's, geeft Gladstone een nauw samenwerkingsverband met UCSF via haar faculteit die gezamenlijke USF benoemingen doet.

Vertaald door Pauline Laumans

( Bron )


Wetenschappers van Gladstone ontdekken methode om giftige eiwitten die geassocieerd worden met Alzheimer te verminderen

Wetenschappers van de Gladstone Institute of Neurological Disease (GIND) hebben nieuwe methodes ontdekt om giftige eiwitten bij Alzheimer te verminderen. Zo ook bij andere neurodegeneratieve ziektes. De resultaten kunnen leiden naar nieuwe behandel-methodes voor deze ziekten. "We onderzochten een eiwit genaamd tau, dat zeer betrokken is bij Alzheimer,"zegt Li Gan, PhD, schrijver van de studie. "Tau vormt giftige eiwit ophopingen in de hersenen van Alzheimer patienten." Tau is een gewoon eiwit in het centraal zenuwstelsel waar het helpt om het cytoskelet te stabiliseren dat het maken van zenuwcellen ondersteunt. Veranderingen in tau zorgen voor zenuwdegeneratie in menselijke hersenen, en tau, veranderd door de toevoeging van fosfaatgroepen(p-tau), vormt ophopingen en beschadigt zenuwcellen. Methodes om zenuwcellen te beschermen tegen p-tau zijn hard nodig.

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Seth


Acetylering kan bijdragen aan ontstaan van dementie en Alzheimer

Een nieuwe studie laat zien dat een eiwitverandering kan bijdragen aan het vormen van zenuwcellenbeschadigende neurofibrillaire klitten in de menselijke hersenen. Het onderzoek gepubliceerd door "Cell Press" in de September 23 uitgave van het Neuron journaal, kan leiden naar nieuwe behandelmethodes van neurodegeneratieve ziektes, die het resultaat zijn van pathologische ophopingen van het tau-eiwit. Tau-eiwit is normaal in het centrale zenuwstelsel, waar het helpt om de microtubuli te stabiliseren die het neuronale cytoskelet vormen. Veranderingen in tau worden geassocieerd met dementie en Alzheimer. Ophopingen van gefosforeerd tau-eiwit (p-tau) worden in verband gebracht  met neurodegenerative aandoeningen. Men is nog niet achter de moluculaire mechanismen die ten grondslag liggen aan abnormale tau-ophopingen.

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Seth


Alzheimer ontstaat door ontregelde stofwisseling zink en ijzer

AlzheimerpatiŽnten kampen met eiwitafzettingen, of 'plaques', in hun hersenen die voor een groot deel bestaan uit het eiwit APP (amyloÔde precusor proteÔne).

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'Alzheimer' is simpelweg een 'doorstromingsprobleem'

1. Zorg dat uw lichaam in 90į functioneert,
2. dat het weefsel genoeg vocht binnenkrijgt van kop tot teen,
3. dat alle wervels en botten 'los' blijven draaien

zodat u uw eigen afval van kop tot teen kunt verwerken' en eer geen 'placques' ontstaat;
de oorsprong van alle moderne ziekten.

Lees verder

Mag ik me nu ook 'onderzoeker' noemen ?

'heerlijke tijdverspillers' toch die meisjes en jongens die - in opdracht van de 'Farma & Co + het grote geld-, maar BLIJVEN onderzoeken....naar zaken die al EEUWEN bekend zijn...en ervoor zorgen dat de ziektekosten ONBETAALBAAR zijn geworden, omdat zij 'simpele dingen' door al hun gestudeer niet meer kunnen bevatten. En ook nog eens mensen volledig BUITEN de samenleving laten belanden. Zouden ze dat nu echt niet in de gaten hebben ?

Ditta


Alzheimer door Hongerwinter?

Hongersnood tijdens de zwangerschap kan leiden tot hersenproblemen bij het kind

Lees verder


B12, foliumzuur en B6 een middel tegen Alzheimer


Vitamine B vermindert kans op Alzheimer

Dagelijkse inname van vitamine B verkleint de kans op geheugenverlies. Dit blijkt uit nieuw onderzoek van de Universiteit van Oxford.

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De Alzheimer-connectie

Tekenen wijzen op een toenemende belangstelling voor de Alzheimer-bijwerkingen bij intens psychoticagebruik (jonge dementen). Al laat het gespecialiseerde milieu voorlopig toch na, die bijwerkingen als een comorbiditeit van ADHD of depressie te noemen. Zoals eerder wel gebeurde met agressief of psychotisch gedrag, zelfmoordgedrag, hallucinaties en al het moois, waarmee met neuroleptica kan gecorrigeerd worden. Bijna een jaar geleden (december 2009) begon men aan VUmc (Amsterdam) jonge 'vasculaire' Alzheimers op te nemen, sinds bleek dat vroege dementie wel eens zou kunnen ontstaan door hersencellen, die gedood werden omdat een chronische vasoconstrictie hen de zuurstof niet kon aanvoeren om te blijven leven. Als de medische wetenschap wel het werkingsmechanisme van de gebruikte psychotica bij ADHD en depressies zou willen kennen, zou de link misschien vlugger gelegd kunnen worden. Hoe ikzelf meer dan twee jaar geleden de link naar de Alzheimer-connectie heb gevonden, staat te lezen in de nieuwsbrief van 1 juni 2008. Ik steunde daarbij op gepubliceerde literatuur, die evenwel zelf naliet om de gepaste conclusies te trekken. Een tijdbom onder antidepressiva en ADHD-medicatie?

Fernand Haesbrouck

Link


Een Alzheimer-pandemie zal door XTC ontstaan zijn

XTC helpt net zo goed bij depressie en ADHD als de psychotica van artsen en de bijwerkingen zijn net zo ziektemakers, die het medisch vak in stand houden.

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Fernand Haesbrouck


Studies richten zich op amyloid plaques en tau tangles

Studies bekijken amyloid plaques (= proteÔneklonters, hersenafwijkingen bij Alzheimer - nvdv) en tau tangles (= anderssoortige proteÔnekluwens, ook bij Alzheimer -nvdv). Een recente internationale conferentie richtte de focus op verschillende kluwenstructuren en plaques binnen neuronen (= zenuwcellen).

Link

Nelly Busschots


Groothoofdigheid kan bescherming bieden tegen symptomen van Alzheimer

Volgens recent onderzoek hebben groothoofdige Alzheimer-patiŽnten een beter geheugen en meer denkvaardigheden dan Alzheimer-patiŽnten met een kleiner hoofd, zelfs al hebben ze hetzelfde aantal dode hersencellen tengevolge van die ziekte. Dit onderzoek werd in het julinummer (13/07/10 - medisch tijdschrift - neurologie) van de American Academy of Neurology gepubliceerd.

Link

Nelly Busschots


Opsnuiven van insuline kan helpen bij de ziekte van Alzheimer

Het opsnuiven van een lage dosis insuline door patiŽnten met de ziekte van Alzheimer geeft een verbetering van de verstandelijke en geheugenfunctie.

Link

Jan Slemmer


Stappen voorwaarts in strijd tegen Alzheimer

De Groningse onderzoekers Marcelo Masman en Ivica Granic hebben hoopvolle ontdekkingen gedaan in de strijd tegen de ziekte van Alzheimer. Masman ontwikkelde een potentieel nieuw medicijn dat het ziekteproces van Alzheimer in een vroeg stadium kan bestrijden. Granic toonde bij muizen aan dat dit medicijn in staat is om geheugenverlies te remmen. Ook ontdekte hij dat het cholesterolverlagende middel Lovastatine bescherming kan bieden tegen het afsterven van zenuwcellen in de hersenen.

De ziekte van Alzheimer kent een complex ziektebeeld, waarbij beschadiging van de hersencellen leidt tot dramatische achteruitgang van geheugen, emoties en denkprocessen. De ziekte wordt onder meer veroorzaakt door samenklontering van het amyloid-beta eiwit, wat dodelijk is voor zenuwcellen in de hersenen. ‘De nu beschikbare medicijnen kunnen de voortgang van Alzheimer enigszins vertragen, maar stoppen het afbraakproces niet,’ zegt Masman. ‘Ons potentieel nieuwe medicijn kan de oorzaak van de ziekte bij de wortel aanpakken.’

Masman ontwikkelde peptiden (korte aminozurenketens) die de vorming van de toxische samenklontering tegengaan en daarmee de giftige uitwerking op hersenweefsel kunnen voorkomen. De peptiden zijn eerst onderzocht in geavanceerde computermodellen, waarmee het ziekteproces zo realistisch mogelijk kan worden nagebootst. ‘Op die manier kon ik verschillende scenario’s simuleren. Ik heb me erop gericht om ťcht te begrijpen wat er gebeurt tijdens het ziekteproces. Ik heb de sterke en zwakke punten van het amyloid-beta eiwit in kaart gebracht, zodat ik vervolgens een peptide kon ontwikkelen dat in staat is een gerichte aanval op het eiwit te doen.’

Masman werkte tijdens zijn onderzoek nauw samen met zijn collegapromovendus Ivica Granic, die verschillende nieuwe therapeutische strategieŽn in de preventie van de ziekte van Alzheimer ontwikkelde en evalueerde. ‘Op basis van de uitkomsten van de computermodellen heb ik de meest succesvolle peptiden getest op hun vermogen om hersencellen te beschermen,’ zegt Granic. ‘Pas nadat we relatief zeker wisten dat ons ontwerp zou werken, heeft Granic het medicijn getest op kweekcellen en muizen,’
aldus Masman. ‘Daaruit bleek dat onze ontdekking zeer effectief is in het voorkomen van hersenschade en de daarmee samenhangende geheugenuitval.’

Granic ontdekte daarnaast dat het cholesterolverlagende middel ‘Lovastatine’ alsook zogeheten ‘calpaineremmers’ de potentie hebben om in te grijpen in het ziekteproces van Alzheimer. ‘Ik heb medicijnen getest die een deel van de fundamentele oorzaken van Alzheimer bestrijden,’ legt Granic uit. ‘Uit mijn onderzoek blijkt onder meer dat Lovastatine en calpaineremmers ook voor een deel bescherming kunnen bieden tegen het afsterven van zenuwcellen in de hersenen en het daarmee gepaard gaande
geheugenverlies. Dat is een stap in goede richting. Mogelijk kan deze ontdekking leiden tot de ontwikkeling van een nieuw medicijn.’

Beide promovendi zijn verheugd met de recente ontwikkelingen, maar benadrukken dat de strijd tegen de ziekte van Alzheimer nog lang niet is gestreden. ‘We moeten erg voorzichtig zijn met de uitkomsten van ons onderzoek. Het is geen magie,’ aldus Masman. ‘Het medicijn is ook nog niet op mensen getest. Deze ontwikkeling heeft zeker potentie, maar het kan nog wel vijftien tot twintig jaar duren voor er echt een
medicijn op de markt komt.’


Appelsap en Alzheimer

Het dagelijks drinken van twee glazen appelsap kan de stemmingswisselingen verbeteren die de ziekte van Alzheimer karakteriseren.

Link

Jan Slemmer


AlzheimerpatiŽnten meer zuurstoftekort

PatiŽnten met de ziekte van Alzheimer lopen meer zuurstoftekort in de hersenschors op bij bloeddrukdaling.

Link


Nieuwe Alzheimer genen ontdekt

Onderzoekers aan de School voor Geneeskunde, Universiteit van Boston, hebben 2 nieuwe genen ontdekt die mogelijk risicofactoren vormen voor een late ontwikkeling van de ziekte van Alzheimer.

Link

Nelly Busschots


Alzheimer wordt veroorzaakt door o.a. aluminium, pesticiden.....
een uitzending die stoort !

Gisteravond 17/05/2010 op France 3: Gif in de kraan. Een onthullende uitzending over het effect van teveel aluminium in het water (van vele inwoners van Frankrijk). Nitraten, pesticiden, medicijnen........Alzheimer is het gevolg. Voor diegenen die Frans spreken: een aanrader.

Link

Ditta


Stress, depressie en vroege symptomen van de ziekte van Alzheimer

In haar proefschrift onderzocht Lotte Gerritsen met behulp van twee grote epidemiologische cohorten of psychosociale stress en depressie gerelateerd zijn aan vroege symptomen van de ziekte van Alzheimer, zoals atrofie van de hersenen en cognitieve achteruitgang.

Stress en depressie kunnen gepaard gaan met veranderingen in stresshormoonniveaus en stresshormonen worden verondersteld schadelijk te zijn voor de hersenen. Maar uit het onderzoek blijkt niet dat psychosociale stress, zoals het doorgemaakt hebben van ernstige levensgebeurtenissen in de jeugd of in het recente verleden, het cognitief functioneren verslechteren. Ook bleek geen verband tussen een depressie en atrofie van de hersenen.

Hogere niveaus van stresshormonen waren wel gerelateerd aan achteruitgang van geheugencapaciteiten, maar alleen bij personen met een genetische kwetsbaarheid voor de ziekte van Alzheimer. Tevens waren verhoogde stresshormonen niveaus geassocieerd met Alzheimer-specifieke hersenatrofie. Deze bevindingen stonden echter los van het doorgemaakt hebben van ernstige levensgebeurtenissen of een depressie.

Dit onderzoek geeft dus geen aanwijzingen dat stresshormonen de relatie tussen psychosociale stress en vroege symptomen van de ziekte van Alzheimer verklaren.


Het vechten tegen de bloedhersen barriŤre kan progressie van de ziekte van Alzheimer vertragen

Onderzoekers kunnen een stap dichter bij komen bij het vertragen van de progressie van de ziekte van Alzheimer. Uit een studie bij dieren ondersteund door de National Institute of Environmental Health Sciences (NIEHS), onderdeel van de National Institutes of Health blijkt dat door zich te richten op de bloed-hersenbarriŤre, onderzoekers in staat zijn om de ophoping van een eiwit die in verband staat met de progressie van de ziekte te vertragen. De bloed-hersenbarriŤre scheidt het circulerend bloed van de hersenen en het beschermt de hersenen door het verwijderen van toxische metabolieten en eiwitten gevormd in de hersenen en blokkade van de toegang van giftige chemische stoffen uit het bloed. "Deze studie kan de experimentele basis bieden voor nieuwe strategieŽn die gebruikt kunnen worden om behandeling van de ziekte van Alzheimer patiŽnten, "zei David S. Miller, Ph.D., hoofd van de Laboratorium voor Toxicologie en farmacologie aan NIEHS en een auteur over de papier dat verschijnt in het mei-nummer van de Moleculaire Farmacologie. Alzheimer is een onomkeerbaar, progressieve hersenaandoening die langzaam het geheugen en denkvermogen vernietigt, en uiteindelijk de functie van belangrijke organen verstoort . De schattingen variŽren, maar deskundigen wijzen erop dat maar liefst 2,6 miljoen tot 5,1 miljoen Amerikanen de ziekte van Alzheimer hebben .

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Eric van Staalduinen


Dement door ‘donuts’?

Pogingen om de ziekte van Alzheimer te behandelen door eiwitplaques in stukjes te hakken, zouden een averechts effect kunnen hebben. Misschien zijn het namelijk juist de kleine brokstukken die het meest schadelijk zijn. Ook de geestelijke achterstand van DownpatiŽnten zou hierdoor te verklaren zijn.

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Verdediging tegen infecties zou ziekte van Alzheimer kunnen activeren

Nieuw onderzoek legt een verband tussen bŤta-amyloÔd, het eiwit dat een rol speelt bij de ziekte van Alzheimer, en eiwitten van het immuunsysteem in de hersenen. Herseninfecties zouden de ziekte van Alzheimer kunnen bevorderen.

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Jan Slemmer


Vaccin tegen Alzheimer

Het aangekondigd vaccin brengt een komende Alzheimer-pandemie in het vooruitzicht. Merkwaardig hoe een en ander in de plooitjes lijkt te vallen.

Niemand schijnt de oorzaak van Alzheimer te (willen) kennen en hoe gaat men Alzheimer te keer? Juist … met een vaccinatie (Het Alzheimer-vaccin (GSK)van Affiris AG ). Een Alzheimerpandemie is de maak en healthcare is eens te meer overtuigd dat die binnenkort zal uitbreken. Aan universitaire centra zijn immers al departementen opgericht om jonge dementen op te vangen. Zie ook mijn nieuwsbrieven 160 en 161.(archief staat op mijn blog, rechtse kolom onderaan) Onbegrijpelijk dat men zogezegd met een vaccin zal proberen het boeltje op te ruimen dat men heeft veroorzaakt door jarenlang antidepressiva of ADHD-medicatie en zelfs Alzheimer medicatie toe te dienen. De amyloidplakken (het boeltje) zijn doodgewoon het 'vuil' dat werd achtergelaten, na de verwoesting in de hersenen door de doping bij depressies en bij ADHD. Zou men er niet beter voor zorgen dat Alzheimer of dementie niet meer kan ontstaan als bijwerking op lange termijn van zeer winstgevende doping.

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Fernand Haesbrouck


Onderzoeker ontdekt hoe foutieve eiwitvouwing plaatsvindt

Nieuw perspectief voor medicijn tegen BSE en Alzheimer

Nieuwe testen die onthullen hoe foutieve eiwitvouwing plaatsvindt, vormen een belangrijke ontdekking waarmee op termijn wellicht medicijnen ontwikkeld kunnen worden tegen prionziektes zoals de gekke koeienziekte (BSE) en de ziekte van Creutzfeldt-Jacob (CJD) of vergelijkbare eiwitstapelingsziekten zoals de ziekte van Alzheimer. Ronald Boshuizen ontwikkelde deze nieuwe testen. Op woensdag 10 maart promoveert hij op dit onderwerp aan de faculteit Diergeneeskunde van de Universiteit Utrecht. Verkeerd vouwende eiwitten die vervolgens gaan stapelen, spelen een belangrijke rol in de ontwikkeling hersenaandoeningen zoals de gekkekoeienziekte (BSE), de ziekte van Creutzfeldt-Jacob (CJD) of de ziekte van Alzheimer. Ronald Boshuizen ontwikkelde testen om inzicht te krijgen in de structuur van de gestapelde prioneiwitten. Met het verkregen inzicht heeft hij korte stukjes eiwit ontworpen waarmee de ongewenste stapeling gestopt kan worden.

Fout eiwit

Eiwitten zijn de bouwstenen en de regelaars van een biologisch systeem. Alle eiwitten hebben een specifieke vorm om hun taken te kunnen uitvoeren. In het 'productieproces' van eiwitten zijn er meerdere systemen die er voor zorgen dat ze de gewenste vorm aannemen. Soms gaat dat fout en kan een ziekte zich ontwikkelen. Prionen, de ziekteverwekkers van BSE en de ziekte van Creutzfeldt-Jacob, zijn foutief gevouwen versies van eiwitten die onder andere in het hersenweefsel voorkomen. Het eiwit in de verkeerd gevouwen vorm werkt als een mal die het goed gevouwen eiwit in de foutieve vorm dwingt. Het uiteindelijke resultaat is het afsterven van hersencellen.

Fundament

Op basis van Boshuizens bevindingen over hoe de foutieve vouwing van eiwitten plaatsvindt, kunnen medicijnen ontwikkeld worden die deze foutieve stapeling kunnen blokkeren. Een opmerkelijk resultaat is dat de foutieve vouwing eerst gestimuleerd moet worden, voordat de stapeling van de fout gevouwen eiwitten te remmen is met een daarvoor speciaal ontworpen stukje eiwit. Wanneer deze strategie van stimuleren en remmen om een prionziekte te stoppen klinisch effect heeft, kan zij wellicht ook toegepast worden bij andere aandoeningen die veroorzaakt worden door foutief vouwende eiwitten.


Veelbelovende nieuwe neuroimaging technieken voor vroegtijdige ontdekking van Alzheimer

Onderzoekers van het "International Centre of Biomedicine" en de Universiteit van Chili, hebben, in samenwerking met het Centrum voor Bioinformatica op de Universiteit van Talca, ontdekt dat twee medicijnen, het benzimidazole derivaat lanzoprazole en astemizole, mogelijk geschikt zijn voor gebruik als PET (positieve elektron afgifte tomografie) opsporing. Hierdoor wordt zichtbaarheid mogelijk gemaakt, zodat Alzheimer in een vroeg stadium kan worden opgespoord.

De studie is gepubliceerd in de meest recente uitgave van de "Journal of Alzheimer's Disease. Lanzoprazole en astemizole hechten zich vooral aan pathologische oligomeren van tau, die de kern van de neurofibrillary tangles (NFT) vormen.  NFT's zijn typerende hersenbeschadigingen bij patiŽnten met de ziekte van Alzheimer. De auteurs van de studie; Prof. Dr. R.B. Maccioni en Dr. Leonel Rojo, "Aangezien de relatie tussen neurofibrillary tangles en hersenbeschadiging bevestigd is, gaan we ervan uit dat deze geneesmiddelen een grote potentie hebben voor (in vivo) vroegtijdige opsporing van Alzheimer en de beperking van vorming van NFT's.

Deze studies, gebaseerd op geavanceerde proteomics en databases van moleculaire interacties, kunnen helpen nieuwe medicijnen te vinden om Alzheimer in een vroeg stadium op te sporen. De bevindingen zijn het resultaat van een reeds lang gevestigd onderzoeksprogramma, gesteund door
de Alzheimerīs Association-USA en Fondecyt, Chile, om nieuwe mogelijke medicijnen te evalueren." Technologische toepassingen van deze ontdekking worden ontwikkeld in samenwerking met Venturel@b van de Adolfo Ibanez Universiteit.

Interessant genoeg binden lanzoprazole en astemizole, al eerder goedgekeurd voor behandeling van proton pomp aandoeningen en respectievelijk als antihistamine, zich ook direct aan opgehoopte varianten van het tau eiwit; in paren lopende, spiraalvormige fijne draden (PHF's) en NFTs in door
Alzheimer aangetaste hersenen. Tot op heden was het niet mogelijk om deze pathologische hersenstructuren in levende Alzheimer patiŽnten op te sporen. De enige bevestiging van de ziekte werd verkregen door postmortale neuropathologische evaluatie. : Link

Vertaling: Inge Hendriks, www.leeffit.nl

Uitleg bij de tekst: Tangles zijn onoplosbare, gedraaide vezels, die voorkomen in de cellen van de hersenen. Deze klitten bestaan voornamelijk uit het eiwit tau. Dit eiwit vormt een bepaalde structuur, de zogenaamde microtubuli. De microtubule helpt voedingsstoffen en andere belangrijke stoffen te vervoeren uit een deel van de zenuwcel naar het andere deel. Bij de ziekte van Alzheimer, is echter het tau-eiwit abnormaal vervormd, waardoor de microtubule structuren instorten.


Neuronen uit huidcellen bieden nieuwe hoop voor AlzheimerpatiŽnten

Amerikaanse wetenschappers hebben voor de eerste keer uit huidcellen neuronen gemaakt, schrijft the Sunday Times.

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Kokosolie voor de ziekte van Alzheimer

Hen & Yan

Ketones: The YouTube Interviews

There is now available on www.YouTube.com a six part series of interviews about ketones, coconut oil and MCT oil and the potential benefits for people with Alzheimer's, Parkinson's and other neurodegenerative diseases. The primary purpose of making these videos is to increase awareness of the need for funding for large scale production of the ketone ester made by Dr. Richard Veech at the NIH. My secondary goal is to let people know that the medium chain triglycerides in coconut oil and MCT oil can produce circulating ketones that can act as an alternative fuel for brain and other cells that
are insulin resistant and cannot use glucose as a fuel; the levels are considerably lower than those that can be achieved with Dr. Veech's ketone ester, however, some improvement or stabilization of disease may still be possible with the oils.

FAST FACTS

Learn more

• Dr. Mary Newport's Web site: www.coconutketones.com

• Accera's information on Axona: www.accerapharma.com

• The Alzheimer's Association statement on medical foods: www.alz.org/national/documents/statements_medicalfoods.pdf

• Caregiver discussions about coconut oil, MCT oil and Axona can be found at http://alzheimers.infopop.cc/eve. (For a key word search, click on the purple "Find'' button at the top of the list.)

http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/63910335/p/1

http://coconutketones.blogspot.com/


Video - Dr. Russel Blaylock on Alex Jones

Dr. Russell Blaylock, a former board certified neurosurgeon, health practitioner, author, lecturer, and newsletter editor.


MRI brengt risico op ziekte van Alzheimer in kaart

Beeldvormende technieken zoals MRI zijn een steeds belangrijker middel voor een vroege diagnose van de ziekte van Alzheimer.

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Marjan


Video - Myelin model for Alzheimer's proposed

A U.S. researcher suggests his "myelin model" -- based on a sheath that covers nerve axons -- is cause for rethinking Alzheimer's disease.


Diagnose van de ziekte Alzheimer met biomarkers is betrouwbaar

Een van de meest veel belovende methoden voor een vroege diagnose van de ziekte van Alzheimer is het meten van specifieke eiwitten (biomarkers) in hersenvocht. Uit een lange-termijn onderzoek van VUmc blijkt dat de meest gebruikte biomarkers, amyloid beta en tau, inderdaad betrouwbare informatie opleveren bij het stellen van de diagnose ziekte van Alzheimer. Voorwaarde is wel dat ervaren laboratoria de metingen uitvoeren. De basis voor onderzoek naar een zo vroeg mogelijke diagnose voor deze ziekte is hiermee verstevigd. Cees Mulder promoveerde op het onderzoek 'biomarkers voor de ziekte van Alzheimer' op 11 november bij VU medisch centrum. De officiŽle diagnose 'Ziekte van Alzheimer' kan pas laat in het ziekte proces worden vastgesteld. Te laat om de ontwikkeling van de ziekte te volgen, eventuele behandelingen te ontwikkelingen en deze toe te passen. Onderzoek naar methoden om de diagnose tijdens het leven in een zo vroeg mogelijk stadium te kunnen stellen, is essentieel om een behandeling te vinden voor deze ziekte. Mulder onderzocht verschillende aspecten van de meting van biomarkers, zoals de opslag van afgenomen hersenvocht en de gebruikte meetmethoden voor het bepalen van de concentraties. De promotie van Mulder (64) is de kroon op zijn werk bij VU medisch centrum. Mulder is sinds 1971 werkzaam bij de organisatie en werkt sinds het begin bij de afdeling klinische chemie onder leiding van prof. dr. M.A. Blankenstein.


Eerste stap naar Alzheimer bij kinderen is gezet.

Studies tonen al aan dat neuronen van Alzheimers er net zo uitzien als die van kinderen of depressieven onder stimulantia behandeling. Maar die studies blijven verborgen.

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Fernand Haesbrouck


Nieuwe aanknopingspunten voor onderzoek Parkinson en Alzheimer

Veel ziekten van het centrale zenuwstelsel gaan gepaard met ophoping van eiwit in de hersenen. Door de genen op te sporen die hierbij betrokken zijn hopen onderzoekers dit proces te kunnen beÔnvloeden. Het promotieonderzoek van Tjakko van Ham lijkt interessante nieuwe aanknopingspunten te bieden voor nader onderzoek naar verouderingsziekten. Het leverde een model op voor de ziekte van Parkinson.
Ook vond hij in een modelorganisme genen die inzicht geven in de moleculaire oorzaak van de ziekte. De onderzoeksresultaten zijn voorgelegd aan een internationaal
wetenschappelijk tijdschrift.


Hoe het ziekenhuis 'omgaat' met AlzheimerpatiŽnt

Fragment uit het VTM-nieuws van 31 augustus 2009: 62 jarige AlzheimerpatiŽnt verdwaalt 3 dagen in het Jan Palfijn ziekenhuis te Gent.


The Alzheimer's Project: Momentum in Science


Copper Damages Protein that Defends Against Alzheimer’s

Copper can damage a molecule that escorts out of the brain a substance called amyloid beta that builds up in toxic quantities in the brains of people with Alzheimer’s disease. The new findings demonstrate one way in which copper might contribute to the development of the disease, though scientists say much more research needs to be done to clarify what role, if any, copper ultimately plays.

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Depression is a risk factor rather than early sign of Alzheimer's disease

A new study by researchers at Rush University Medical Center supports the idea that depression is truly a risk factor for Alzheimer's disease rather than a subtle early sign of its underlying pathology. The study, published in the April issue of the Archives of General Psychiatry, found no evidence of an increase in depressive symptoms during the prodromal phase before the clinical diagnosis of Alzheimer's disease.

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Hormone shows promise in reversing Alzheimer's disease and stroke

Saint Louis University researchers have identified a novel way of getting a potential treatment for Alzheimer's disease and stroke into the brain where it can do its work. "We found a unique approach for delivering drugs to the brain," says William A. Banks, M.D., professor of geriatrics and pharmacological and physiological science at Saint Louis University. "We're turning off the guardian that's keeping the drugs out of the brain." The brain is protected by the blood-brain barrier (BBB), a gate-keeping system of cells that lets in nutrients and keeps out foreign substances. The blood-brain barrier passes no judgment on which foreign substances are trying to get into the brain to treat diseases and which are trying to do harm, so it blocks them without discrimination. "The problem in treating a lot of diseases of the central nervous system – such as Alzheimer's disease, HIV and stroke – is that we can't get drugs past the blood-brain barrier and into the brain," says Banks, who also is a staff physician at Veterans Affairs Medical Center in St. Louis. "Our new research shows a way of getting a promising treatment for these types of devastating diseases to where they need to be to work." The therapy – known as PACAP27 -- is a hormone produced by the body that is a general neuro-protectant. PACAP stands for pituitary adenylate cyclase-activating polypeptide. "It is a general protector of the brain against many types of insult and injury," Banks says. He compares a specific guarding mechanism in the BBB -- efflux pumps – to bouncers at exclusive nightclubs. While they welcome those on the approved guest list, they look for trouble-makers trying to crash the party, refuse to let them in and evict them if they do get in.

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Author Pratchett blames his Alzheimer's on mercury fillings

Terry Pratchett has reopened the controversy about the safety of mercury-based tooth fillings by blaming them for his Alzheimer's disease. The author of the Discworld series describes the fillings - which millions of Britons have - as "toxic waste".

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How neural sludge accumulates in Alzheimer's

Researchers have identified a key mechanism by which the protein sludge that kills brain cells accumulates in Alzheimer's disease. Their findings in mice offer clues to treating AD and also could explain why memory centers of the brain are most affected in the disease.

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A simple balance test may predict cognitive decline in Alzheimer's disease

A simple balance test may predict cognitive decline in Alzheimer's Disease, according to a study published in the March 2009 issue of the Journal of Alzheimer's Disease. This study was carried out in 16 university hospital departments of neurology, geriatrics or psychiatry in ten cities with 686 outpatients suffering from AD. This population is representative of the AD population seen by clinicians in daily practice. Patients were evaluated by a geriatrician every six months for up to two years, and their degree of cognitive impairment was measured using the Mini Mental State Examination (MMSE). At the same time, a "one-leg balance" (OLB) test was given, where a participant was asked to stand on one leg for as long as possible. The OLB test was reported as abnormal when the participant was unable to stand on one leg for 5 seconds or more. Participants with an abnormal OLB at baseline or/and during the follow-up showed significantly more cognitive decline at 12, 18 and 24 months than the participants with a OLB test normal at baseline and normal during the follow-up. The worst condition (having an abnormal OLB at baseline and during the follow-up= no improvement) was associated with a mean adjusted cognitive decline of 9.2 points. The best condition (having a normal OLB at baseline and during the follow-up = no worsening) was associated with a mean adjusted cognitive decline of 3.8 points.

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Pittsburgh Compound B finds Alzheimer’s-associated plaques in symptom-free older adults

In the largest study of its kind, Pittsburgh Compound B, an imaging agent that could facilitate the early diagnosis of Alzheimer's disease, has been used to identify amyloid deposition in the brains of clinically older adults. The findings, published in this month's issue of the Archives of Neurology, could not only shed more light on how the illness progresses, but also open the door to the possibility of prevention strategies, said senior investigator William E. Klunk, M.D., Ph.D., professor of psychiatry and neurology at the University of Pittsburgh School of Medicine. He and study co-author Chester A. Mathis, Ph.D., a Pitt professor of radiology and pharmaceutical sciences, invented the imaging compound, dubbed PiB. It binds to certain forms of amyloid protein plaques that are thought to destroy brain cells and have been found in the brains of Alzheimer's disease patients. Before PiB, the deposits could only be identified during autopsy to confirm the diagnosis in hindsight. Results of the study, which was led by Howard J. Aizenstein, M.D., Ph.D., associate professor of psychiatry and bioengineering at Pitt, "show that we can detect amyloid deposits before patients develop symptoms of Alzheimer's disease," Dr. Klunk said. "That means we might have a window of opportunity to slow or stop the process."

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Anesthesia Is Found To Induce Hyperphosphorylation of Tau at Sites Related to Alzheimer’s Disease

Scientists from The New York State Office of Mental Retardation and Developmental Disabilities’ (OMRDD) New York State Institute for Basic Research in Developmental Disabilities (IBR) report today in the March 2009 issue of the Journal of Alzheimer’s Disease that anesthesia induces phosphorylation of tau. Tau is a key neuronal protein involved in neurodegeneration in Alzheimer’s disease (AD) and several other neurodegenerative disorders. Anesthesia has previously been found to be associated with cognitive impairment and the risk for AD. This study helps elucidate the molecular mechanisms underlying these associations. The researchers found that in test animals, anesthesia for short periods (30 seconds to 5 minutes) induced tau phosphorylation at some selective phosphorylation sites to a small but significant extent. Anesthesia for a longer time (1 hour) induced much more dramatic phosphorylation at the same sites, possibly as a result of anesthesia-induced hypothermia. The observation that anesthesia did not induce global hyperphosphorylation of brain proteins, but instead specific hyperphosphorylation of tau protein at the AD-related abnormal hyperphosphorylation sites suggests that tau hyperphosphorylation might be the mechanism that links anesthesia and the risk of cognitive impairment and/or AD. AD is the most common cause of dementia in adults and affects approximately 27 million individuals worldwide and over four million in the United States alone. Most AD cases are sporadic and are believed to be caused by multiple factors. Understanding the mechanism by which anesthesia may increase the risk for cognitive impairment will help in the design of strategies for preventing and treating dementia and AD. “This is a very important finding related to Alzheimer’s disease,” said OMRDD Commissioner Diana Jones Ritter. “I am pleased that these findings will lead to helping people live richer lives through the research findings.”

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Potatoes may hold key to Alzheimer's treatment

A virus that commonly infects potatoes bears a striking resemblance to one of the key proteins implicated in Alzheimer's disease, and researchers have used that to develop antibodies that may slow or prevent the onset of AD.

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Common anesthetic induces Alzheimer's-associated changes in mouse brains

For the first time researchers have shown that a commonly used anesthetic can produce changes associated with Alzheimer's disease in the brains of living mammals, confirming previous laboratory studies. In their Annals of Neurology report, which has received early online release, a team of Massachusetts General Hospital (MGH) investigators shows how administration of the gas isoflurane can lead to generation of the toxic amyloid-beta (A-beta) protein in the brains of mice. "These are the first in vivo results indicating that isoflurane can set off a time-dependent cascade inducing apoptosis [cell death] and enhanced levels of the Alzheimer's-associated proteins BACE and A-beta," says Zhongcong Xie, MD, PhD, of the MassGeneral Institute for Neurodegenerative Disease (MGH-MIND) and the MGH Department of Anesthesia and Critical Care, the study's lead and corresponding author. "This work needs to be confirmed in human studies, but it's looking like isoflurane may not be the best anesthesia to use for patients who already have higher A-beta levels, such as the elderly and Alzheimer's patients." Alzheimer's disease is characterized by deposition of A-beta plaques within the brain. The A-beta protein is formed when the larger amyloid precursor protein (APP) is clipped by two enzymes – beta-secretase, also known as BACE, and gamma-secretase – to release the A-beta fragment. Normal processing of APP by an enzyme called alpha-secretase produces an alternative, non-toxic protein. Several studies have suggested that surgery and general anesthesia may increase the risk of developing Alzheimer's disease, and it is well known that a small but significant number of surgical patients experience a transient form of dementia in the postoperative period. Last year the MGH team showed that applying isoflurane to cultured neural cells increased activation of the cell-death protein caspase and raised levels of BACE and gamma-secretase as part of a pathway leading to the generation of A-beta. The current study was designed to see if the same process takes place in mice.

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Study suggests blood test for Alzheimer’s possible

Researchers have revealed a direct relationship between two specific antibodies and the severity of Alzheimer’s disease symptoms, raising hopes that a diagnostic blood test for the devastating disorder is within reach.Researchers from the University of Georgia, the Charlie Norwood VA Medical Center in Augusta and the Medical College of Georgia compared antibody levels in blood samples from 118 older adults with the participant’s level of dementia. The team, whose results appear in the current edition of Journal of Gerontology: Medical Sciences, found that the concentration of two specific proteins that are involved in the immune response increases as the severity of dementia increases."We found a strong and consistent relationship between two particular antibodies and the level of impairment,” said study co-author L. Stephen Miller, professor and director of clinical psychology training in the UGA Franklin College of Arts and Sciences. “The finding brings us closer to our ultimate goal of developing a blood test that can diagnose Alzheimer’s disease or potentially identify if someone is at higher risk for the disease.”

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LSUHSC research identifies key contributor to Alzheimer's disease process

Walter J. Lukiw, PhD, Associate Professor of Neuroscience and Ophthalmology at LSU Health Sciences Center New Orleans, is the lead author of a paper identifying, for the first time, a specific function of a fragment of ribonucleic acid (RNA), once thought to be no more than a byproduct, in regulating inflammation and the development of Alzheimer's disease. The paper, An NF-kB-sensitive micro RNA-146a-mediated inflammatory circuit in Alzheimer's disease and in stressed human brain cells, will be published in the November 14, 2008 issue of The Journal of Biological Chemistry. Dr. Lukiw's lab at the LSU Health Sciences Center New Orleans Neuroscience Center of Excellence has shown that this tiny piece of RNA, or microRNA, called miRNA-146a is found in increased amounts in stressed human brain cells and in Alzheimer's disease, and that it plays a crucial role in the regulation of inflammation and disease-related neuropathology thought to be integral to the Alzheimer's disease process. Dr. Lukiw's research team, which also included LSUHSC's Jian Guo Cui, MD, PhD and Yuhai Zhao, a post doctoral student in the lab, demonstrated in human brain cells in primary culture that MiRNA-146a targets the messenger RNA of an important anti-inflammatory regulator called complement factor H (CFH). Testing both control cells and Alzheimer's disease-affected tissues, they found that miRNA-164a appears to reduce the amount and bioavailability of CFH, promoting the inflammation of brain cells and contributing to the development of Alzheimer's disease.

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Brain damage found in cognitively normal people with Alzheimer's marker

Researchers at Washington University School of Medicine in St. Louis have linked a potential indicator of Alzheimer's disease to brain damage in humans with no signs of mental impairment. Although their cognitive and neurological assessments were normal, study participants with lower levels of a substance known as amyloid beta 42 (A-beta 42) in their cerebrospinal fluid (CSF) had reduced whole brain volumes, suggesting that Alzheimer's changes might already be damaging their brains. Scientists previously showed that low CSF levels of A-beta 42 mark the presence of amyloid deposition in the brain, a key diagnostic marker of the amyloid plaques that characterize Alzheimer's disease. Evidence is mounting that Alzheimer's harms the brain for many years before physicians and family members can detect symptoms, and this has led many to conclude that successful Alzheimer's treatments may only be possible if scientists find ways to identify pre-symptomatic sufferers. The results are an encouraging sign that this search for new indicators, known as antecedent biomarkers, may be succeeding, according to senior author David M. Holtzman, M.D., the Andrew and Gretchen Jones Professor and chair of the Department of Neurology at the School of Medicine and neurologist-in-chief at Barnes-Jewish Hospital. "We still need to confirm with long-term follow-up studies that subjects with this biomarker and brain damage go on to develop the cognitive changes characteristic of Alzheimer's," says Holtzman. "For now, the evidence we've uncovered further proves that identification and treatment prior to the start of the symptoms of Alzheimer's disease are likely going to be essential to preventing irreversible brain injury."

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Vitamin E May Help Alzheimer’s Patients Live Longer

People with Alzheimer's disease who take vitamin E appear to live longer than those who don't take vitamin E, according to research that will be presented at the American Academy of Neurology 60th Anniversary Annual Meeting in Chicago, April 12–19, 2008. For the study, researchers followed 847 people with Alzheimer's disease for an average of five years. About two-thirds of the group took 1,000 international units of vitamin E twice a day along with an Alzheimer’s drug (a cholinesterase inhibitor). Less than 10 percent of the group took vitamin E alone and approximately 15 percent did not take vitamin E. The study found people who took vitamin E, with or without a cholinesterase inhibitor, were 26 percent less likely to die than people who didn't take vitamin E.

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Biomarkers for Alzheimer's disease can be trusted in clinical trials

The best-established biomarkers for Alzheimer's disease have a low natural variation over two years. The results speak for the inclusion of these biomarkers in clinical trials of novel drugs against Alzheimer's disease.

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Alzheimer’s Starts Earlier for Heavy Drinkers, Smokers

Heavy drinkers and heavy smokers develop Alzheimer’s disease years earlier than people with Alzheimer’s who do not drink or smoke heavily, according to research that will be presented at the American Academy of Neurology 60th Anniversary Annual Meeting in Chicago, April 12–19, 2008. “These results are significant because it’s possible that if we can reduce or eliminate heavy smoking and drinking, we could substantially delay the onset of Alzheimer’s disease for people and reduce the number of people who have Alzheimer’s at any point in time,” said study author Ranjan Duara, MD, of the Wien Center for Alzheimer’s Disease at Mount Sinai Medical Center in Miami Beach, FL, and Fellow of the American Academy of Neurology.

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Children's Hospital Oakland scientist finds potential Alzheimer's cure in century-old drug

A new study conducted by researchers at Children's Hospital & Research Center Oakland shows that a century-old drug, methylene blue, may be able to slow or even cure Alzheimer's and Parkinson's disease. Used at a very low concentration – about the equivalent of a few raindrops in four Olympic-sized swimming pools of water - the drug slows cellular aging and enhances mitochondrial function, potentially allowing those with the diseases to live longer, healthier lives. A paper on the methylene blue study, conducted by Hani Atamna, PhD, and a his team at Children's, was published in the March 2008 issue of the Federation of American Societies for Experimental Biology (FASEB) Journal. Dr. Atamna's research found that methylene blue can prevent or slow the decline of mitochondrial function, specifically an important enzyme called complex IV. Because mitochondria are the principal suppliers of energy to all animal and human cells, their healthy function is critical. "The results are very encouraging," said Dr. Atamna. "We'd eventually like to try to prevent the physical and cognitive decline associated with aging, with a focus on people with Alzheimer's disease. One of the key aspects of Alzheimer's disease is mitochondrial dysfunction, specifically complex IV dysfunction, which methylene blue improves. Our findings indicate that methylene blue, by enhancing mitochondrial function, expands the mitochondrial reserve of the brain. Adequate mitochondrial reserve is essential for preventing age-related disorders such as Alzheimer's disease."

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Another McGill/JGH breakthrough opens door to early Alzheimer's diagnosis

A new diagnostic technique which may greatly simplify the detection of Alzheimer's disease has been discovered by researchers at McGill University and the affiliated Lady Davis Institute for Medical Research at Montreal's Jewish General Hospital (JGH). Their results were published June 8 in the Journal of Alzheimer's Disease. There is currently no accepted blood test for Alzheimer's, and the diagnosis is usually based on expensive and labour-intensive neurological, neuropsychological and neuroimaging evaluations. Dr. Hyman Schipper and colleagues at the Lady Davis Institute and McGill University utilized a new minimally-invasive technique called near-infrared (NIR) biospectroscopy to identify changes in the blood plasma of Alzheimer's patients, changes which can be detected very early after onset, and possibly in pre-clinical stages of the disease. Biospectroscopy is the medical form of spectroscopy, the science of detecting the composition of substances using light or other forms of energy. In NIR spectroscopy, different substances emit or reflect light at specific, detectable wavelengths.

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Pipex test confirms copper involvement in Alzheimer's disease

Pipex Pharmaceuticals has announced positive clinical results of Alzheimer's disease test that used FreeBound, Pipex's proprietary pharmacodiagnostic device for measurement of serum free and total copper. The test demonstrated the significance of copper in Alzheimer's disease.

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A novel way found to prevent protein plaques implicated in Alzheimer's

For unknown reasons a protein called amyloid beta aggregates into toxic plaques in the brain, killing neurons. These plaques are one of the hallmarks of Alzheimer's disease. Now two new animal studies show for the first time that the deadly transformation of amyloid beta into plaques can be prevented through an interaction between amyloid beta and another protein called cystatin C.

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Calcium’s Possible Role In Alzheimer’s

A new study in mice finds that plaques associated with Alzheimer’s wreak havoc on calcium’s role in cell signaling. Careful journalists write that Alzheimer’s disease is associated with the characteristic plaques in patients’ brains, never that it’s caused by those plaques.

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LSUHSC research reports new method to protect brain cells from diseases like Alzheimer's

New research led by Chu Chen, PhD, Associate Professor of Neuroscience at LSU Health Sciences Center New Orleans, provides evidence that one of the only naturally occurring fatty acids in the brain that has the ability to interact with the receptors originally identified as the targets of THC (the psychoactive component of marijuana) can help to protect brain cells from neurodegenerative diseases like Alzheimer's and Parkinson's. Published in the August 15, 2008 issue of the Journal of Biological Chemistry, the research focuses on the cellular and molecular mechanisms of inflammation, specifically the role these relatively recently discovered endogenous cannabinoids can play in the control of COX-2 and other cyclooxygenases. COX-2 is a key player in neuroinflammation and has been implicated in the development of neurodegenerative diseases and worsening of damage from such insults as traumatic brain injury and stroke.Chen and research associate Jian Zhang show that endocannabinoid 2-arachidonoylglycerol (2-AG) functions as an endogenous COX-2 inhibitor, turning off the production of COX-2 which normally goes into overdrive in response to pro-inflammatory and certain types of toxic stimuli, resulting in the injury or death of brain cells. The researchers also revealed the specific signaling pathways that regulate the 2-AG suppression of COX-2. The paper, Endocannabinoid 2-Arachidonoylglycerol Protects Neurons by Limiting COX-2 Elevation, is available online at http://www.jbc.org.

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Brain damage found in cognitively normal people with Alzheimer's marker

Researchers at Washington University School of Medicine in St. Louis have linked a potential indicator of Alzheimer's disease to brain damage in humans with no signs of mental impairment. Although their cognitive and neurological assessments were normal, study participants with lower levels of a substance known as amyloid beta 42 (A-beta 42) in their cerebrospinal fluid (CSF) had reduced whole brain volumes, suggesting that Alzheimer's changes might already be damaging their brains. Scientists previously showed that low CSF levels of A-beta 42 mark the presence of amyloid deposition in the brain, a key diagnostic marker of the amyloid plaques that characterize Alzheimer's disease. Evidence is mounting that Alzheimer's harms the brain for many years before physicians and family members can detect symptoms, and this has led many to conclude that successful Alzheimer's treatments may only be possible if scientists find ways to identify pre-symptomatic sufferers.

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Anesthesia and Alzheimer's

In studies of human brain cells, the widely-used anesthetic desflurane does not contribute to increased production of amyloid-beta protein; however, when combined with low oxygen conditions, it can produce more of this Alzheimer's associated protein.

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Compounds Have Potential For Diagnosis, Treatment Of Alzheimer's Disease

Scientists have discovered that these compounds interact in three specific ways with the tau protein, which is the subject of a growing body of research into the causes and progression of dementia.In a normal, healthy brain, the tau protein binds to and stabilizes structures in the brain that are essential for proper functioning. But tau protein that breaks away from these structures can begin forming long strands called filaments. These filaments can clump into tangles, which are a marker of Alzheimer’s disease and other neurodegenerative disorders. Depending on the specific compounds under study, they can produce three different outcomes when introduced to the tau protein: They either bind to the protein filaments; inhibit the filaments from developing; or drive tau protein to form filaments. So far, the interactions have been observed in test tubes and cell cultures, so any clinical use of the compounds will require years of additional research.

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Coatings To Help Medical Implants Connect With Neurons

Plastic coatings could someday help neural implants treat conditions as diverse as Parkinson's disease and macular degeneration. The coatings encourage neurons in the body to grow and connect with the electrodes that provide treatment. Jessica O. Winter, assistant professor of chemical and biomolecular engineering at Ohio State University described the research Thursday, August 21 at the American Chemical Society meeting in Philadelphia. She is also an assistant professor of biomedical engineering. Worldwide, researchers are developing medical implants that stimulate neurons to treat conditions caused by neural damage. Most research focuses on preventing the body from rejecting the implant, but the Ohio State researchers are focusing instead on how to boost the implants' effectiveness.

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Alzheimer's Disease Neuroimaging Initiative announces completion of genome-wide analysis

Researchers announced today that a high-density genome wide analysis of participants in the Alzheimer's Disease Neuroimaging Initiative (ADNI; www.adni-info.org) is more than 95% complete and that data will be shared with scientists around the world for further analysis. The ADNI data will be used by researchers to search for genes that contribute to the development of Alzheimer's disease, which currently affects up to 5 million people in the United States alone. ADNI, an ongoing $60 million project, is a public-private partnership supported primarily by the National Institutes of Health (NIH) with pharmaceutical and related industries and not-for-profit organizations providing support through the Foundation for the National Institutes of Health (FNIH). One of the largest scale neuroimaging projects ever undertaken, ADNI involves longitudinal magnetic resonance imaging (MRI) and positron emission tomography (PET) brain imaging and blood, urine and spinal fluid biomarker studies of more than 800 individuals, half of whom have mild cognitive impairment, a condition placing them at high risk for developing Alzheimer's disease or another dementia. The primary goal of ADNI is to determine whether brain imaging, other biological markers, and clinical and neuropsychological assessment can accurately measure the progression of mild cognitive impairment and early Alzheimer's disease. The identification of specific biomarkers of early Alzheimer's disease and disease progression will provide a useful tool for researchers and clinicians in both the diagnosis of early Alzheimer's disease and in the development, assessment and monitoring of new treatments. One major Alzheimer's disease risk gene, APOE, has been consistently shown to be associated with the form of the disease arising later in life that accounts for approximately 95 percent of all cases. It is widely suspected that variants in an ensemble of other genes play a role in susceptibility to the disease and may influence the age of onset, expression and rate of progression of neurodegenerative changes in the brain. "This new data set provides a unique opportunity to evaluate the associations between a highly comprehensive dataset based on brain imaging, clinical examinations and other biomarkers and the entire genome or selected candidate genes," said Andrew Saykin, Psy.D., director of the IU Center for Neuroimaging at the Indiana University School of Medicine, who leads the genetics research team.

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Novel approach to treat Alzheimer's and other diseases offered by targeting cell membrane RAFTS

This week in Science magazine, researchers from JADO Technologies, with colleagues at the Max Planck Institute and others, report on a potential new strategy for targeting Alzheimer's by inhibiting Ŗ-secretase, the enzyme involved in plague formation. This new strategy hitchhikes onto a natural cellular mechanism called RAFT that allows a Ŗ-secretase inhibitor to be anchored via a proprietary sterol linker into endosomes, the precise location where Ŗ-secretase is most active and exerts its neurotoxic activity.

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Possible new Alzheimer's gene identified

A variant of the gene CDC2 could possibly be used as a risk marker for Alzheimer's disease. The gene variant is considerably more common among Alzheimer's patients. This is shown in a dissertation from the Sahlgrenska Academy at GŲteborg University in Sweden. Alzheimer's disease has several different causes. Since many patients have a close relative who also developed the disease, heredity is believed to be one of the most important factors.

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Study Confirms Validity of Pittsburgh Compound-B in Identifying the Toxins Associated with Alzheimer’s Disease

A groundbreaking study conducted by University of Pittsburgh Alzheimer’s disease researchers reported in the journal Brain (currently online) confirms that Pittsburgh Compound-B (PiB) binds to the telltale beta-amyloid deposits found in the brains of patients with Alzheimer’s disease. The finding is a significant step toward enabling clinicians to provide a definitive diagnosis of Alzheimer’s disease in living patients.

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Automated analysis of MR images may identify early Alzheimer’s disease

Analyzing MRI studies of the brain with software developed at the Martinos Center for Biomedical Imaging at Massachusetts General Hospital (MGH) may allow diagnosis of Alzheimer's disease and of mild cognitive impairment, a lesser form of dementia that precedes the development of Alzheimer's by several years. In their report that will appear in the journal Brain and has been released online, the MGH/Martinos team show how their software program can accurately differentiate patients with mild cognitive impairment or Alzheimer's disease from normal elderly individuals based on anatomic differences in brain structures known to be affected by the disease. "Traditionally Alzheimer's has been diagnosed based on a combination of factors – such as a neurologic exam, detailed medical history and written tests of cognitive functioning – with neuroimaging used primarily to rule out other diseases such as stroke or a brain tumor," says Rahul Desikan MD, PhD, of the Martinos Center and Boston University School of Medicine, lead author of the Brain paper. "Our findings show the feasibility and importance of using automated, MRI-based neuroanatomic measures as a diagnostic marker for Alzheimer's disease." The researchers note that mild cognitive impairment occurs in about 20 percent of elderly individuals – as many as 40 percent of those over 85 – 80 percent of whom develop Alzheimer's within five or six years. Since drugs that may slow the progression of Alzheimer's are in development, the ability to treat patients in the earliest stages of the disease may significantly delay progression to dementia. To investigate whether MR imaging can produce diagnostic markers for mild cognitive impairment and Alzheimer's disease, the research team used FreeSurfer – an openly available imaging software package developed at the Martinos Center and the University of California at San Diego – to examine a number of neuroanatomic regions across a range of normal individuals and patients with mild cognitive impairment and Alzheimer's disease.

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Cerebrospinal fluid shows AlzheimerŅs disease deterioration much earlier

It is possible to determine which patients run a high risk of developing Alzheimer’s disease and the dementia associated with it, even in patients with minimal memory impairment. This has been shown by recent research at the Sahlgrenska Academy.The results have been published in the most recent issue of the prestigious medical journal Lancet Neurology. "The earlier we can catch Alzheimer’s disease, the more we can do for the patient. The disease is one that progresses slowly, and the pharmaceuticals that are currently available are only able to alleviate the symptoms", says Kaj Blennow, professor at the Sahlgrenska Academy, and a world?leading researcher in the field.

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Mechanism of Alzheimer's suggests combination therapy needed

Researchers at the University of Illinois at Chicago College of Medicine have discovered a mode of action for mysterious but diagnostic protein snarls found in the brains of Alzheimer's patients that suggests a one-two punch of therapy may be needed to combat the neurodegenerative disease. Alzheimer's disease, which may affect as many as 5 million Americans and is among the most costly diseases to society in the United States and Europe, is characterized by two distinctive protein malformations: amyloid plaques and tau tangles. Amyloid plaques are sticky deposits made up of a short protein called amyloid beta, and tau tangles are made of short filaments of the tau protein. So far no one has been able to explain how amyloid beta and the tau tangles wreak their damage on the nervous system. "We have known for a long time that amyloid beta was bad," said Scott Brady, professor and head of anatomy and cell biology at the UIC College of Medicine. "What we haven't understood is why it's bad." The findings, reported in a new study appearing in the Proceedings of the National Academy of Sciences Online Early Edition for March 16-20, suggest promising new targets for combination therapy. In previous work, published earlier this year, the researchers suggested how tau tangles work together with amyloid beta to create a perfect storm that destroys neural function and memory. "Cell death occurs at a very late stage of the disease," said Brady, principal investigator of the study. "Long before the cells die they lose function, and that function is critical for the symptoms that we see." Brady and his colleagues found that when short assemblies of amyloid -- rather than the long-chain plaques -- get inside neurons, they interfere with the cells' transport system. This limits their ability to send vital proteins and vesicles to where they are needed within the cell and interferes with the synaptic connections to other nerve cells.

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Low level of conscientiousness may be a risk factor for Alzheimer's disease

Individuals who are more conscientious -- in other words, those with a tendency to be self-disciplined, scrupulous and purposeful -- appear less likely to develop Alzheimer's disease, according to a report in the October issue of Archives of General Psychiatry, one of the JAMA/Archives journals.

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New project uses nanoparticles to tackle Alzheimer's disease

A new EU-funded project is exploring the use of nanoparticles in the diagnosis and treatment of Alzheimer's disease. The five-year NAD ('Nanoparticles for the therapy and diagnosis of Alzheimer's disease') initiative has a budget of €14.6 million and is financed by the EU's Seventh Framework Programme (FP7). It brings together researchers from a variety of disciplines working in 19 organisations in 13 countries. The NAD project will design a range of nanoparticles that are able to cross the blood-brain barrier to get to the main site of the disease. Attached to these nanoparticles will be molecules that are able to recognise and destroy the amyloid plaques. Initial studies will be carried out on transgenic mice; if these prove successful, tests will be carried out on human subjects.

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Study links diabetes and Alzheimer's disease

Diabetic individuals have a significantly higher risk of developing Alzheimer's disease but the molecular connection between the two remains unexplained. Now, researchers at the Salk Institute for Biological Studies identified the probable molecular basis for the diabetes -- Alzheimer's interaction.

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Researchers Seeking to Identify Alzheimer’s Risk with New Biomarkers Make Significant Progress by Focusing on a Specific Blood Marker

A simple blood test to detect whether a person might develop Alzheimer’s disease is within sight and could eventually help scientists in their quest toward reversing the disease’s onset in those likely to develop the debilitating neurological condition, Columbia University Medical Center researchers announced today. Building on a study that started 20 years ago with an elderly population in Northern Manhattan at risk or in various stages of developing Alzheimer’s disease, the Columbia research group has yielded ground-breaking findings that could change the way the disease is treated or someday prevent it. These findings suggest that by looking at the blood doctors may be able to detect a person’s predisposition to developing the dementia-inducing disease that robs a person of their memory and ability carry out tasks essential to life.

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Alzheimer's discovery could bring early diagnosis, treatment closer

A discovery made by researchers at McGill University and the affiliated Lady Davis Research Institute for Medical Research at Montreal's Jewish General Hospital offers new hope for the early diagnosis and treatment of Alzheimer's disease. In a study published in the Journal of Biological Chemistry on May 15, Dr. Hemant Paudel, his PhD student Dong Han and postdoctoral fellows Hamid Qureshi and Yifan Lu, report that the addition of a single phosphate to an amino acid in a key brain protein is a principal cause of Alzheimer's. Identifying this phosphate, one of up to two-dozen such molecules, could make earlier diagnosis of Alzheimer's possible and might, in the longer term, lead to the development of drugs to block its onset. The crucial protein, called a tau protein, is a normal part of the brain and central nervous system. But in Alzheimer's patients, tau proteins go out of control and form tangles that, along with senile plaques, are the primary cause of the degenerative disease. Several years ago, it was discovered that tau proteins in normal brains contain only three to four attached phosphates, while abnormal tau in Alzheimer's patients have anywhere from 21 to 25 additional phosphates. Paudel and his team have discovered that it is the addition of a single phosphate to the Ser202 amino acid within the tau brain protein that is the principal culprit responsible for Alzheimer's. "The impact of this study is twofold," said Paudel, associate professor at McGill's Dept. of Neurology and Neurosurgery, and Project Director at the Bloomfield Centre for Research in Aging at the Lady Davis. "We can now do brain imaging at the earliest stages of the disease. We don't have to look for many different tau phosphates, just this single phosphate. The possibility of early diagnosis now exists. "Second, the enzyme which puts this phosphate on the tau can be targeted by drugs, so therapies can be developed. This discovery gives us, for the first time, a clear direction towards the early diagnosis and treatment of Alzheimer's."

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Alzheimer's Disease Could Be Triggered by Brain Toxins

But emerging evidence indicates that toxic environmental exposures, in combination with nutritional, social, and exercise factors, may play a major role in the development of Alzheimer’s disease, Parkinson’s disease, and other chronic degenerative diseases, according to Philip Landrigan, MD.

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Rapid changes in key Alzheimer's protein described in humans

For the first time, researchers have described hour-by-hour changes in the amount of amyloid beta, a protein that is believed to play a key role in Alzheimer's disease, in the human brain. A collaborative team of scientists at Washington University School of Medicine in St. Louis and the University of Milan report their results this week in Science. "Proving that we can directly measure amyloid beta in the human brain is an important step forward for both clinical and basic research, and that may be true not just in Alzheimer's disease but also in other serious neurological disorders," says co-first author David L. Brody, M.D., Ph.D., a Washington University neurologist who treats brain injury and general neurology patients at Barnes-Jewish Hospital. The results of the study contradicted the expectations of researchers, who were hoping to learn why brain injury is linked to higher risk of Alzheimer's disease. They had hypothesized that such injuries, caused by motor vehicle accidents, assaults and falls, would lead to an increase in amyloid beta levels. Instead, they found recovery from brain injury, rather than the injury itself, seemed to increase amyloid. The better a patient's overall neurological status, the higher their amyloid beta levels rose."We can't at this point rule out a very early spike in amyloid right after a brain injury," notes Brody, assistant professor of neurology. "This study is just the beginning."

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Cholesterol metabolism links early- and late-onset Alzheimer's disease

Researchers at Washington University School of Medicine in St. Louis have uncovered evidence strengthening the case for another potential cause of Alzheimer's. The finding also represents the first time scientists have found a connection between early- and late-onset Alzheimer's.

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Green vegetables might hold clue to Alzheimer's

Deficiencies in the levels of folate in the blood can triple a person's risk of developing Alzheimer's and other forms of dementia, according to researchers. Folate, which is also known as vitamin B9, is found in most dark green vegetables.

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Treating Alzheimer`s - through the nose

For Prof. Beka Solomon it was obvious. If it isn`t possible to send drugs to the brain to treat Alzheimer`s disease the normal way because of the blood-brain barrier that prevents drugs from moving from the blood stream into the brain, then send them through the nose instead. Solomon, of the Molecular Microbiology and Biotechnology Department at Tel Aviv University, has been working in this field for the last 13 years after years of research in immunotherapy, and found in mouse trials that filamentous phages, a harmless bacterial virus found almost everywhere from the depths of the ocean to the lining of the stomach, can be an effective treatment against Alzheimer`s disease when carried to the brain through the nose.

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International TGen-led team finds link between brain protein and Alzheimer's disease

Investigators at the Translational Genomics Research Institute (TGen) today announced a link between the brain protein KIBRA and Alzheimer's disease, a discovery that could lead to promising new treatments for this memory-robbing disorder. The new discovery builds on a previous TGen-led study published in the prestigious journal Science, which showed a genetic link between KIBRA and memory in healthy adults. In the new study, TGen researchers found that carriers of a memory-enhancing flavor of the KIBRA gene had a 25 percent lower risk of developing Alzheimer's disease. The findings were reported Saturday in the online edition of Neurobiology of Aging, a Philadelphia-based peer-review journal that generally focuses on how aging affects the nervous system. "This research suggests that KIBRA, and possibly some of the proteins with which it interacts, may play a role in Alzheimer's disease," said Dr. Matthew Huentelman, an investigator in TGen's Neurogenomics Division and the paper's senior author.

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MBL researchers discover a mechanism of neurodegeneration in Alzheimer's disease

Tiny, toxic protein particles severely disrupt neurotransmission and inhibit delivery of key proteins in Alzheimer's disease, two separate studies by Marine Biological Laboratory (MBL) researchers have found. The particles are minute clumps of amyloid beta, which has long been known to accumulate and form plaques in the brain of Alzheimer's patients. "These small particles that haven't aggregated into plaques—these are increasingly being seen as the really toxic species of amyloid beta," says Scott Brady of University of Illinois College of Medicine, who has been an MBL investigator since 1982. Brady and his colleagues found that these particles inhibit neurons from communicating with each other and with other target cells in the body. "The disease symptoms for Alzheimer's are associated not with the death of the neurons – that is a very late event – but with the loss of functional connections. It's when the neuron is no longer talking to its targets that you start to get the memory deficits and dementia associated with the disease," Brady says. The amyloid beta particles activate an enzyme, CK2, which in turn disrupts the "fast axonal transport" system inside the neuron, Brady found. This transport system has motor proteins that move various kinds of cargo (including neurotransmitters and the associated protein machinery for their release) from place to place in the neuron on microtubule tracks. Brady's findings are complemented by a new study by Rudolfo LlinŠs of New York University School of Medicine. Brady and LlinŠs both conduct neuroscience research at the MBL using the giant nerve cell of the Woods Hole squid, Loligo paeleii, as a model system.

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Cerebrospinal fluid shows Alzheimer's disease deterioration much earlier

It is possible to determine which patients run a high risk of developing Alzheimer’s disease and the dementia associated with it, even in patients with minimal memory impairment. This has been shown by recent research at the Sahlgrenska Academy, University of Gothenburg, Sweden. The results have been published in the most recent issue of the prestigious medical journal Lancet Neurology. "The earlier we can catch Alzheimer’s disease, the more we can do for the patient. The disease is one that progresses slowly, and the pharmaceuticals that are currently available are only able to alleviate the symptoms", says Kaj Blennow, professor at the Sahlgrenska Academy, and a world?leading researcher in the field. Several biomarkers have been identified in recent years. Biomarkers are proteins that can be detected in the cerebrospinal fluid and used to diagnose Alzheimer’s disease. It is now clear that the typical pattern of biomarkers known as the "CSF AD profile" can be seen in the cerebrospinal fluid of patients even with very mild memory deficiencies, before these can be detected by other tests.

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Is vitamin D deficiency linked to Alzheimer's disease and vascular dementia?

There are several risk factors for the development of Alzheimer's disease and vascular dementia. Based on an increasing number of studies linking these risk factors with Vitamin D deficiency, an article in the current issue of the Journal of Alzheimer's Disease (May 2009) by William B. Grant, PhD of the Sunlight, Nutrition, and Health Research Center (SUNARC) suggests that further investigation of possible direct or indirect linkages between Vitamin D and these dementias is needed. Low serum levels of 25-hydroxyvitamin D [25(OH)D] have been associated with increased risk for cardiovascular diseases, diabetes mellitus, depression, dental caries, osteoporosis, and periodontal disease, all of which are either considered risk factors for dementia or have preceded incidence of dementia. In 2008, a number of studies reported that those with higher serum 25(OH)D levels had greatly reduced risk of incidence or death from cardiovascular diseases. Several studies have correlated tooth loss with development of cognitive impairment and Alzheimer's disease or vascular dementia. There are two primary ways that people lose teeth: dental caries and periodontal disease. Both conditions are linked to low vitamin D levels, with induction of human cathelicidin by 1,25-dihydroxyvitamin D being the mechanism. There is also laboratory evidence for the role of vitamin D in neuroprotection and reducing inflammation, and ample biological evidence to suggest an important role for vitamin D in brain development and function.

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Researchers find 1 in 6 women, 1 in 10 men at risk for Alzheimer's disease in their lifetime

Researchers from Boston University School of Medicine have estimated that one in six women are at risk for developing Alzheimer's disease in their lifetime, while the risk for men is one in ten. These findings were released today by the Alzheimer's Association in their publication 2008 Alzheimer’s Disease: Facts and Figures.

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New mechanism for amyloid beta protein's toxic impact on the Alzheimer's brain

Scientists have uncovered a novel mechanism linking soluble amyloid ? protein with the synaptic injury and memory loss associated with Alzheimer's disease (AD). The research, published by Cell Press in the June 25 issue of the journal Neuron, provides critical new insight into disease pathogenesis and reveals signaling molecules that may serve as potential additional therapeutic targets for AD. Amyloid ? protein (A?) plays a major pathogenic role in AD, a devastating neurodegenerative disorder characterized by progressive cognitive impairment and memory loss. "Given the mounting evidence that small soluble A? assemblies mediate synaptic impairment in AD, elucidating the precise molecular pathways by which this occurs has important implications for treating and preventing the disease," explains senior study author, Dr. Dennis Selkoe from the Center for Neurologic Diseases at Brigham and Women's Hospital and Harvard Medical School. Dr. Selkoe, Dr. Shaomin Li, and colleagues examined regulation of a cellular communication phenomenon known as long-term synaptic depression (LTD). LTD has been linked with neuronal degeneration, but a role for A? in the regulation of LTD has not been clearly described. The researchers found that soluble A? facilitated LTD in the hippocampus, a region of the brain intimately associated with memory. The enhanced synaptic depression induced by soluble A? was mediated through a decrease in glutamate recycling at hippocampal synapses. Excess glutamate, the major excitatory neurotransmitter in the brain, is thought to contribute to the progressive neuronal loss characteristic of AD. The researchers went on to show that A?-enhanced LTD was mediated by glutamate receptor activity and that the LTD could be prevented by an extracellular glutamate scavenger system. A very similar enhancement of LTD could be induced by a pharmacological blocker of glutamate reuptake. Importantly, soluble A? directly and significantly decreased glutamate uptake by isolated synapses. "Our findings provide evidence that soluble A? from several sources enhances synaptic depression through a novel mechanism involving altered glutamate uptake at hippocampal synapses," concludes Dr. Selkoe. "These results have both mechanistic and therapeutic implications for the initiation of hippocampal synaptic failure in AD and in more subtle forms of age-related A? accumulation." Future studies are needed to determine precisely how soluble A? protein physically interferes with glutamate transporters at the synapse.

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Innovative 3D-imaging technique captures brain damage linked to Alzheimer's disease

Using an advanced three-dimensional mapping technique developed by UCLA researchers, the team analyzed magnetic resonance imaging data from 24 patients with amnestic mild cognitive impairment and 25 others with mild Alzheimer's disease. The research team found that patients with mild Alzheimer's had 10 to 20 percent more atrophy in most cortical areas than did MCI patients.

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UIC chemists characterize Alzheimer's neurotoxin structure

Associate professor of Chemistry Yoshitaka Ishii and his team have isolated an intermediate structure of the fiber-like amyloid plaques (fibrils) which, they believe, can be responsible for the nerve cell damage associated with Alzheimer's.

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Study Suggests Link Between Smoking and Alzheimer’s

a new study conducted by Frank M. LaFerla, associate director of the Institute for Brain, Aging and Dementia at UC Irvine, shows that nicotine may contribute to Alzheimer’s disease, despite previous research suggesting that nicotine may prevent the crippling disease.

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Alzheimer's disease linked to mitochondrial damage

Investigators at Burnham Institute for Medical Research (Burnham) have demonstrated that attacks on the mitochondrial protein Drp1 by the free radical nitric oxide—which causes a chemical reaction called S-nitrosylation—mediates neurodegeneration associated with Alzheimer's disease. Prior to this study, the mechanism by which beta-amyloid protein caused synaptic damage to neurons in Alzheimer's disease was unknown. These findings suggest that preventing S-nitrosylation of Drp1 may reduce or even prevent neurodegeneration in Alzheimer's patients. The paper was published in the April 3 issue of the journal Science. The team of scientists, led by neuroscientist and clinical neurologist Stuart A. Lipton, M.D., Ph.D., director of the Del E. Webb Center for Neuroscience, Aging and Stem Cell Research, showed that S-nitrosylated Drp1 (SNO-Drp1) facilitates mitochondrial fragmentation, damaging regions of nerve cell communication called synapses. Mitochondria are the energy storehouses of the cell, and their compromise by excessive fragmentation causes synaptic injury and eventual nerve cell death. Synapses are critical for learning and memory and their impairment leads to the dementia seen in Alzheimer's patients. "We now have a better understanding of the mechanism by which beta-amyloid protein causes neurodegeneration in Alzheimer's disease," said Dr. Lipton. "We found that beta-amyloid can generate nitric oxide that reacts with Drp1. By identifying Drp1 as the protein responsible for synaptic injury, we now have a new target for developing drugs that may slow or stop the progression of Alzheimer's." Drp1 is an enzyme that mediates fission or fragmentation of mitochondria. The Burnham researchers showed that excessive production of nitric oxide caused S-nitrosylation of Drp1 and induced excessive fragmentation of mitochondria in cultured nerve cells or neurons. The scientists also showed that beta-amyloid protein multimers, which had been previously implicated in Alzheimer's disease, induced formation of SNO-Drp1. Importantly, elevated SNO-Drp1 levels were also found in human brains of Alzheimer's patients, but not in those with Parkinson's disease or controls who didn't have neurodegenerative diseases. Molecular modeling performed by the team suggested that S-nitrosylation of Drp1 causes dimerization of the protein and activation of enzymatic activity that induces mitochondrial fragmentation. To confirm this hypothesis, the scientists showed that RNA interference to knock down Drp1 or a mutation that prevented Drp1 activity inhibited excess mitochondrial fragmentation and protected the neurons. Finally, the researchers showed that a mutated Drp1, lacking the nitrosylation site, did not induce mitochondrial fragmentation and also prevented neuronal damage. Taken together, these findings suggest that multimers of beta-amyloid protein induce generation of nitric oxide, which reacts with Drp1 to cause excessive mitochondrial fragmentation and in turn neuronal damage.

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Paradigm Shift in Alzheimersīs Research opens the Door for New Treatments: Intraneural AŖ aggregation triggers neuron loss

Latest research by Professor Thomas Bayer from University Medicine Center GŲttingen carries the promise of developing new treatments. Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by extensive neuronal degeneration and the development of neuritic amyloid plaques and neurofibrillary tangles. Neuronal and synaptic losses in AD are correlated with dementia and occur in specific brain areas involved in memory processing. Long-standing evidence shows that progressive cerebral deposition of AŖ plays a seminal role in the pathogenesis of AD. There is great interest, therefore, in understanding the proteolytic processing of APP, the precursor of AŖ, and its proteases responsible for generating AŖ. Ragged peptides with a major species beginning with phenylalanine at position 4 of Ab have been reported already in 1985 by Masters et al.1.

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Young adults at future risk of Alzheimer's have different brain activity, says study

Young adults with a genetic variant that raises their risk of developing Alzheimer's Disease show changes in their brain activity decades before any symptoms might arise, according to a new brain imaging study by scientists from the University of Oxford and Imperial College London. The results may support the idea that the brain's memory function may gradually wear itself out in those who go on to develop Alzheimer's. The research, published today in the journal Proceedings of the National Academy of Sciences, provides clues as to why certain people develop Alzheimer's Disease (AD) and it may be a step towards a diagnostic test that identifies individuals at risk. The degenerative condition is the most common cause of dementia and it affects around 417,000 people in the UK. The APOE4 genetic variant is found in about a quarter of the population. Not everyone who carries the variant will go on to develop AD, but people who inherit one copy of APOE4 have up to four times the normal risk of developing the late-onset variety of the disease. People who have two copies have around ten times the normal risk. The researchers behind today's study stress that most carriers of APOE4 will not go on to develop Alzheimer's and carriers should not be alarmed by the study's findings.

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Cancer-related protein may play key role in Alzheimer's disease

Researchers describe a new function for the cancer-related protein Akt -- one that may help promote the development of Alzheimer's disease.

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Test quickly assesses whether Alzheimer's drugs are hitting their target

A test developed by physician-scientists at Washington University School of Medicine in St. Louis may help assess more quickly the ability of Alzheimer's drugs to affect one of the possible underlying causes of Alzheimer's disease in humans, accelerating the development of new treatments. Scientists used the test to show that an Alzheimer's drug given to healthy volunteers reduced production of a substance known as amyloid beta (A-beta), a normal byproduct of human metabolism that builds to unhealthy levels forming brain plaques in Alzheimer's patients. The drug candidate, LY450139, which is also known as semagacestat, is being studied in clinical trials by Eli Lilly and Company.Ongoing clinical trials are studying the effect that semagacestat may have on cognitive function and biochemical and brain imaging biomarkers in patients with Alzheimer's disease. Washington University researchers wanted to see whether the new measurement technique, stable isotope-linked kinetics (SILK), could detect the study drug's impact on A-beta synthesis in healthy volunteers. "Bringing an Alzheimer's disease drug into clinical trials from tests in animal models has always been challenging," says study director Randall Bateman, M.D., a Washington University neurologist who treats patients at Barnes-Jewish Hospital. "We haven't had a way to quickly and accurately assess a drug's effects, and that meant there always had to be some degree of educated guesswork when it came to setting the optimal dosage for humans. SILK may help to eliminate much of that guesswork."

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Plaques, Tangles in Brain Don't Always Lead to Alzheimer's

New British research provides more evidence that the bits of gunk in the brain known as plaques and tangles don't necessarily lead to Alzheimer's disease, as many experts have long believed.

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Positive Breakthrough for NuroPro(R) Blood Test for Alzheimer's

This breakthrough, which involved the successful diagnoses of different forms of Alzheimer's, including high-risk patients, was achieved during the initial phase of clinical validation trials of the Company's NuroPro(R) AD blood test.

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Mount Sinai researchers discover novel mechanisms that might causally link type 2 diabetes to Alzheimer's disease

A recent study by Mount Sinai faculty suggests that a gene associated with onset of type-2 diabetes also decreases in Alzheimer's disease dementia cases. The research, led by Dr. Giulio Maria Pasinetti, MD, Ph.D., The Aidekman Family Professor in Neurology, and Professor of Psychiatry and Geriatrics and Adult Development at Mount Sinai School of Medicine, was published this week in the scientific journal, Archives of Neurology. "This new evidence is of extreme interest," Dr. Pasinetti tells us, "especially because of the evidence that approximately 60% of Alzheimer's disease dementia cases have at least one serious medical condition primarily associated with type-2 diabetes, a chronic condition which includes high blood glucose content (hyperglycemia) and reduced sensitivity to insulin, among other conditions." "The relationship between type-2 diabetes and Alzheimer's disease is elusive," says Dr. Pasinetti. Not all subjects with type-2 diabetes are affected by Alzheimer's disease, and similarly, not all Alzheimer's disease cases are diabetic. However, in the last few years, epidemiological evidence indicates that, relative to healthy elderly subjects, people of the same age affected by type-2 diabetes are twice as likely to develop Alzheimer's disease dementia. The reason is not known. The new study from Dr. Pasinetti, reported in this week's issue of Archives of Neurology, provides insight into a potential mechanism that might explain the relationship between type-2 diabetes and Alzheimer's disease onset and progression. Dr. Pasinetti and colleagues found that a gene known as proliferator-activated receptor coactivator 1 - (PGC-1 ), a key regulator of glucose content currently investigated as a potential therapeutic target for type-2 diabetes, is also decreased in Alzheimer' disease dementia cases. Most importantly, Dr. Pasinetti reports that PGC-1 decreased in Alzheimer' disease dementia cases with progression of the clinical disease and positively correlates with brain accumulation of ?-amyloid, an abnormal protein highly linked to Alzheimer' disease dementia and brain degeneration. This evidence is of high interest to the field and suggests, for the first time, a strong relationship between decreased content of a gene responsible for type-2 diabetes in Alzheimer's disease dementia cases, says Dr. Pasinetti.

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Non-drug treatment of Alzheimer’s disease - long-term benefit not proven

Reliable conclusions about the potential for benefit and harm are currently not possible / In general there is still a great need for good studies on non-drug interventions. Whether people with Alzheimer's disease benefit in the long term from non-drug treatment interventions remains an unanswered question. This unsatisfactory finding is mainly due to the fact that convincing studies are lacking so far. For individual approaches, the studies provide indications of a benefit, but also of harm. This is the result of the final report by the Institute for Quality and Efficiency in Health Care (IQWiG) published on 17 March 2009. According to IQWiG, a general problem of the benefit assessment of non-drug treatment interventions is particularly shown in the therapy of Alzheimer's disease: small research budgets and an underdeveloped study methodology lead to the situation that even for procedures with potential, no reliable conclusions can be drawn and thus no proof of a benefit can be provided.

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Umbilical cord blood cell therapy may reduce signs and symptoms of Alzheimer's disease

Targeted immune suppression using human umbilical cord blood cells significantly improved Alzheimer's-like brain damage in a mouse model of the neurodegenerative disease, a new study reports.

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'Largest' Alzheimer's gene study

Researchers are conducting what is believed to be the largest study yet of genes which cause Alzheimer's disease.

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New findings resolve long dispute about how the disease might kill brain cells

For a decade, Alzheimer's disease researchers have been entrenched in debate about one of the mechanisms believed to be responsible for brain cell death and memory loss in the illness. Now researchers at the University of Michigan and the University of California, San Diego have settled the dispute. Resolving this controversy improves understanding of the disease and could one day lead to better treatments. Michael Mayer, an assistant professor in the U-M departments of Biomedical Engineering and Chemical Engineering, and Jerry Yang, an assistant professor in the Department of Chemistry and Biochemistry at UCSD, and their colleagues found a flaw in earlier studies supporting one side of the debate. Their findings are published online in the Journal of Neurotoxicity Research. They will appear in the May print edition. Their results clarify how small proteins called amyloid-beta peptides damage brain cell membranes, allowing extra calcium ions to enter the neurons. An ion is an electrically-charged particle. An ion imbalance in a cell can trigger its suicide. Amyloid-beta peptides are the prime suspects for causing cell death in Alzheimer's, although other mechanisms could also be to blame. The disease is not well understood. The researchers confirmed evidence found by others that amyloid-beta peptides prick pores into brain cell membranes, opening channels where calcium ions can rush in. This was one mechanism the field had contemplated, but other evidence suggested a different scenario. Some researchers believed that the peptide caused a general thinning of the cell membranes and these thinned membranes lost their ability to keep calcium ions out of brain cells. Mayer and Yang disproved this latter theory. "When you understand these mechanisms better, you have a better chance of being able to pharmaceutically counteract them as a possible treatment. For instance, if amyloid-beta thins membranes, this general effect might be difficult to treat. On the other hand, if it forms pores, this effect might be treatable with pore blockers. Ion channel blockers are medications sold today to treat a variety of diseases," Mayer said. He cautions that much research is needed before it is known whether such medications are effective and safe to treat Alzheimer's. Mayer and Yang were able to explain the other experimental results that blamed cell membrane thinning for uncontrolled calcium ion fluctuations. It turns out that in these studies, trace amounts of residual solvent used to prepare the peptide had a dramatic effect. The Michigan- and UCSD-led team reproduced these experimental results using only the solvent, without the peptide. The solvent is called Hexafluoroisopropanol, or HFIP."HFIP is a good solvent used to break up clumps of the peptide to prepare for experiments, but it's toxic and membrane-active. What we found was that the reported preparation procedure did not remove the solvent effectively," Mayer said. "Our findings are watertight since we could reproduce the thinning effect in the absence of amyloid-beta peptides by this solvent alone."

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Study validates Pittsburgh Compound-B in identifying Alzheimer's disease brain toxins

A groundbreaking study conducted by University of Pittsburgh Alzheimer's disease researchers reported in the journal Brain (currently online) confirms that Pittsburgh Compound-B binds to the telltale beta-amyloid deposits found in the brains of patients with Alzheimer's disease. The finding is a significant step toward enabling clinicians to provide a definitive diagnosis of Alzheimer's disease in living patients.

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Low level of neuronal receptor linked to mild cognitive impairment and Alzheimer's disease

Results of a new study indicate a strong link between the loss of the neuronal receptor LR11and onset of mild cognitive impairment (MCI), often a harbinger of Alzheimer's disease. The findings also show that levels of LR11 in the brain tissue reflect the severity of cognitive impairment and may predict which individuals will progress to Alzheimer's disease.

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Study Confirms Validity of Pittsburgh Compound-B in Identifying the Toxins Associated with Alzheimer’s Disease

A groundbreaking study conducted by University of Pittsburgh Alzheimer’s disease researchers reported in the journal Brain (currently online) confirms that Pittsburgh Compound-B (PiB) binds to the telltale beta-amyloid deposits found in the brains of patients with Alzheimer’s disease. The finding is a significant step toward enabling clinicians to provide a definitive diagnosis of Alzheimer’s disease in living patients.

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Smokers are more likely to develop dementia

People who smoke are more likely to develop Alzheimer's disease or dementia than nonsmokers or those who smoked in the past, according to a study published in the Sept. 4, 2007, issue of Neurology, the medical journal of the American Academy of Neurology.

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Gladstone scientists uncover potential mechanism of memory loss in Alzheimer's disease

Scientists have revealed a potential mechanism by which Amyloid beta, causes neurological disfunction in Alzheimer's patients.

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Mice with Alzheimer's disease suffer 'silent' seizures

Mice genetically engineered to have a disease like Alzheimer's have "silent" seizures that appear related to cellular changes involving the excess accumulations of the protein amyloid beta, said researchers from the Gladstone Institute of Neurological Disease and Baylor College of Medicine in a report that appears in today's issue of the journal Neuron.

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Insulin is a Possible New Treatment for Alzheimer’s

A Northwestern University-led research team reports that insulin, by shielding memory-forming synapses from harm, may slow or prevent the damage and memory loss caused by toxic proteins in Alzheimer’s disease. The findings, which provide additional new evidence that Alzheimer’s could be due to a novel third form of diabetes, will be published online the week of Feb. 2 by the Proceedings of the National Academy of Sciences (PNAS). In a study of neurons taken from the hippocampus, one of the brain’s crucial memory centers, the scientists treated cells with insulin and the insulin-sensitizing drug rosiglitazone, which has been used to treat type 2 diabetes. (Isolated hippocampal cells are used by scientists to study memory chemistry; the cells are susceptible to damage caused by ADDLs, toxic proteins that build up in persons with Alzheimer’s disease.) The researchers discovered that damage to neurons exposed to ADDLs was blocked by insulin, which kept ADDLs from attaching to the cells. They also found that protection by low levels of insulin was enhanced by rosiglitazone. ADDLs (short for “amyloid beta-derived diffusible ligands”) were discovered at Northwestern and are known to attack memory-forming synapses. After ADDL binding, synapses lose their capacity to respond to incoming information, resulting in memory loss.

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Research on link between vitamin D and Alzheimer’s ‘warranted’

A California scientist has been arguing there is a good reason to conduct more in-depth research on the possible causative link between vitamin D levels and the development of Alzheimer’s disease.

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Humanin peptide linked to neuronal cell survival and regulation of glucose metabolism

Recent studies have shown that the mitochondrial peptide Humanin (HN) protects against neuronal cell death such as happens in Alzheimer's disease. Now, in a study presented April 22 at Experimental Biology 2009 in New Orleans, Dr. Nir Barzilai reports that a small infusion of HN is the most potent regulator of insulin metabolism that his research team has ever seen, significantly improving overall insulin sensitivity and sharply decreasing the glucose levels of diabetic rats. The finding is the first evidence of a role for HN in glucose metabolism and provides new insight into how this metabolism may be involved in the development of seemingly diverse age-related diseases such as Type 2 Diabetes Mellitus and Alzheimer's. The finding also provides support for the growing understanding that the brain (not just the pancreas, liver and other peripheral organs) is heavily involved in glucose metabolism. Furthermore, says Dr. Barzilai, the Ingeborg and Ira Leon Rennert Chair of Aging Research and Director of the Institute for Aging Research at the Albert Einstein College of Medicine, the power of HN on insulin action suggests a new therapeutic approach to diabetes. Further understanding of how HN interactions with the growth hormone/insulin-like growth factor system may also lead to strategies to protect against age-related diseases including Alzheimer's.

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Blocking formation of toxic plaques implicated in type 2 diabetes

Amid growing evidence that the same abnormal clumping of proteins in Alzheimer’s disease also contributes to type-2 diabetes, scientists in New York are reporting discovery of a potent new compound that reduces formation of those so-called amyloid plaques. Their study is scheduled for the Sept. 5 issue of the Journal of the American Chemical Society, a weekly publication.The report cites evidence correlating increases in amyloid formation in the pancreas with increases in severity and rate of progression of type-2 diabetes, which affects almost 20 million Americans and is rapidly rising worldwide. Deposits of the abnormal protein damage and destroy insulin-producing “islet” cells in the pancreas. Researchers have been seeking potential new medicines that block formation of an abnormal, misfolded protein called islet amyloid polypeptide (IAPP), which may play a key role in the cell destruction.

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Mediterranean diet may help Alzheimer's patients live longer

A Mediterranean diet may help people with Alzheimer’s disease live longer than patients who eat a more traditional Western diet. The study is published in the September 11, 2007, issue of Neurology, the medical journal of the American Academy of Neurology.

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Mayo Clinic Researchers Find Agents that Speed Up Destruction of Proteins Linked to Alzheimer's Disease

Taking a new approach to the treatment and prevention of Alzheimer's disease, a research team led by investigators at the Mayo Clinic campus in Florida has shown that druglike compounds can speed up destruction of the amyloid beta (A-beta) proteins that form plaque in the brains of patients with the disorder. Researchers say their study, published in the April 22 online issue of PLoS ONE, demonstrates that this strategy is a viable and exciting alternative to the approach most drug designers have taken to date.

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Increased Level Of Magnetic Iron Oxides Found In Alzheimer’s Disease

A team of scientists, led by Professor Jon Dobson, of Keele University in Staffordshire, UK, have found, for the first time, raised levels of magnetic iron oxides in the part of the brain affected by Alzheimer's Disease (AD). Their research has also shown that this association was particularly strong in females compared to males. The group speculates that this may be a result of gender differences in the way the body handles and stores iron. Though the results are based on a small number of samples, they give an indication that iron accumulation associated with Alzheimer's appears to involve the formation of strongly magnetic iron compounds. As these compounds have a strong effect on MRI signal intensity, with further study, it may be possible to use this as a biomarker for the development of an MRI-based Alzheimer's diagnostic technique.

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Study explores computers to detect Alzheimer's in brain scans

Computers can be trained to detect early signs of Alzheimer's disease in MRI brain scans, according to a study from Mayo Clinic and other participating centers. The findings were published in the March 2008 issue of Brain.

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UCSB scientists make headway in understanding Alzheimer's disease

Scientists at UC Santa Barbara have discovered that a protein called BAG2 is important for understanding Alzheimer's disease and may open up new targets for drug discovery. They are ready to move from studying these proteins in culture to finding out how they work with mice. In a paper published this week in the Journal of Neuroscience, the scientists describe important activities of BAG2 in cleaning up brain cells. The protein tau is normally found in brain cells, but scientists don't know why it clumps into tangles in people with Alzheimer's disease. Senior author Kenneth S. Kosik, co-director of UCSB's Neuroscience Research Institute, and Harriman Chair in Neuroscience, has been involved in the study of neurons that develop neurofibrillary tangles, one of the hallmarks of the disease, since he was a postdoctoral fellow. "Early on in my career, we were one of several labs to discover that tau was in the neurofibrillary tangles," said Kosik. Kosik's team recently started to work on BAG2 to find out how it may be involved in the removal of tangled tau. "It turns out that when you put this protein into the cell, it clears away the damaged tau very nicely," said Kosik. It doesn't clear away all the tau; it goes for the damaged tau protein and removes it.

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Researchers find possible environmental causes for Alzheimer's, diabetes

A new study by researchers at Rhode Island Hospital have found a substantial link between increased levels of nitrates in our environment and food with increased deaths from diseases, including Alzheimer's, diabetes mellitus and Parkinson's. The study was published in the Journal of Alzheimer's Disease (Volume 17 - July 2009). Led by Suzanne de la Monte, MD, MPH, of Rhode Island Hospital, researchers studied the trends in mortality rates due to diseases that are associated with aging, such as diabetes, Alzheimer's, Parkinson's, diabetes and cerebrovascular disease, as well as HIV. They found strong parallels between age adjusted increases in death rate from Alzheimer's, Parkinson's, and diabetes and the progressive increases in human exposure to nitrates, nitrites and nitrosamines through processed and preserved foods as well as fertilizers. Other diseases including HIV-AIDS, cerebrovascular disease, and leukemia did not exhibit those trends. De la Monte and the authors propose that the increase in exposure plays a critical role in the cause, development and effects of the pandemic of these insulin-resistant diseases. De la Monte, who is also a professor of pathology and lab medicine at The Warren Alpert Medical School of Brown University, says, "We have become a 'nitrosamine generation.' In essence, we have moved to a diet that is rich in amines and nitrates, which lead to increased nitrosamine production. We receive increased exposure through the abundant use of nitrate-containing fertilizers for agriculture." She continues, "Not only do we consume them in processed foods, but they get into our food supply by leeching from the soil and contaminating water supplies used for crop irrigation, food processing and drinking." Nitrites and nitrates belong to a class of chemical compounds that have been found to be harmful to humans and animals. More than 90 percent of these compounds that have been tested have been determined to be carcinogenic in various organs. They are found in many food products, including fried bacon, cured meats and cheese products as well as beer and water. Exposure also occurs through manufacturing and processing of rubber and latex products, as well as fertilizers, pesticides and cosmetics. Nitrosamines are formed by a chemical reaction between nitrites or other proteins. Sodium nitrite is deliberately added to meat and fish to prevent toxin production; it is also used to preserve, color and flavor meats. Ground beef, cured meats and bacon in particular contain abundant amounts of amines due to their high protein content. Because of the significant levels of added nitrates and nitrites, nitrosamines are nearly always detectable in these foods. Nitrosamines are also easily generated under strong acid conditions, such as in the stomach, or at high temperatures associated with frying or flame broiling. Reducing sodium nitrite content reduces nitrosamine formation in foods. Nitrosamines basically become highly reactive at the cellular level, which then alters gene expression and causes DNA damage. The researchers note that the role of nitrosamines has been well-studied, and their role as a carcinogen has been fully documented. The investigators propose that the cellular alterations that occur as a result of nitrosamine exposure are fundamentally similar to those that occur with aging, as well as Alzheimer's, Parkinson's and Type 2 diabetes mellitus.

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Caffeine reverses memory impairment in Alzheimer's mice

Coffee drinkers may have another reason to pour that extra cup. When aged mice bred to develop symptoms of Alzheimer's disease were given caffeine – the equivalent of five cups of coffee a day – their memory impairment was reversed, report University of South Florida researchers at the Florida Alzheimer's Disease Research Center. Back-to-back studies published online today in the Journal of Alzheimer's Disease, show caffeine significantly decreased abnormal levels of the protein linked to Alzheimer's disease, both in the brains and in the blood of mice exhibiting symptoms of the disease. Both studies build upon previous research by the Florida ADRC group showing that caffeine in early adulthood prevented the onset of memory problems in mice bred to develop Alzheimer's symptoms in old age. "The new findings provide evidence that caffeine could be a viable 'treatment' for established Alzheimer's disease, and not simply a protective strategy," said lead author Gary Arendash, PhD, a USF neuroscientist with the Florida ADRC. "That's important because caffeine is a safe drug for most people, it easily enters the brain, and it appears to directly affect the disease process." Based on these promising findings in mice, researchers at the Florida ADRC and Byrd Alzheimer's Center at USF hope to begin human trials to evaluate whether caffeine can benefit people with mild cognitive impairment or early Alzheimer's disease, said Huntington Potter, PhD, director of the Florida ADRC and an investigator for the caffeine studies. The research group has already determined that caffeine administered to elderly non-demented humans quickly affects their blood levels of ?-amyloid, just as it did in the Alzheimer's mice. "These are some of the most promising Alzheimer's mouse experiments ever done showing that caffeine rapidly reduces beta amyloid protein in the blood, an effect that is mirrored in the brain, and this reduction is linked to cognitive benefit," Potter said. "Our goal is to obtain the funding needed to translate the therapeutic discoveries in mice into well-designed clinical trials."

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New way to diagnose Alzheimer's disease promises earlier treatment

Physicians may be able to detect and treat Alzheimer's in its earliest stages, when patients are experiencing only mild degrees of cognitive impairment, thanks to new diagnostic criteria proposed by an international group of researchers.

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Novel role of protein in generating amyloid-beta peptide

A defining hallmark of Alzheimer's disease is the accumulation of the amyloid ? protein (A?), otherwise known as "senile plaques," in the brain's cortex and hippocampus, where memory consolidation occurs. Researchers at the University of California, San Diego School of Medicine have identified a novel protein which, when over-expressed, leads to a dramatic increase in the generation of A?. Their findings, which indicate a potential new target to block the accumulation of amyloid plaque in the brain, will be published in the May 1 issue of the Journal of Biological Chemistry. "The role of the multi-domain protein, RANBP9, suggests a possible new therapeutic target for Alzheimer's disease," said David E. Kang, PhD, assistant professor of neurosciences at UC San Diego and director of this study. The neurotoxic protein A? is derived when the amyloid precursor protein (APP) is "cut" by two enzymes, ?-secretase (or BACE) and ?-secretase (or Presenilin complex.) However, inhibiting these enzymes in order to stop the amyloid cascade has many negative side effects, as these enzymes also have various beneficial uses in brain cells. So the researchers looked for an alternative way to block the production of amyloid beta. In order for cleavage to occur, the APP needs to travel to cholesterol-enriched sites within the cell membrane called RAFTS, where APP interacts with the two enzymes. It is this contact that the researchers sought to block. Kang explains that the researchers identified the RANBP9 protein by studying low density lipoprotein receptor-related protein (LRP), a protein that rapidly shuttles A? out of the brain and across the blood-brain barrier to the body, where it breaks down into harmless waste products. A small segment of LRP can also stimulate A? generation, and the scientists narrowed this segment down to a 37-amino-acid stretch that can lead to changes in A?. "RANBP9 is one of the proteins we identified that interacted with this LRP segment, but one that had never before been associated with disease-related neuronal changes," said Kang. "We discovered that this protein interacts with three components involved in A? generation – LRP, APP and BACE1 – and appears to 'scaffold' them into a structure." Kang explained that these three components must come together to result in the first cut or cleaving that leads to production of A?. To test this, the scientists knocked out RANBP9 in the cell, and discovered that 60% less A? was produced. "This unique factor enhances the production of beta amyloid," said Kang. "Inhibiting the RANBP9 protein may offer an alternative approach to therapy, by preventing contact between APP and the enzyme that makes the cut essential to produce amyloid plaques." The researchers' next step is to verify these findings in animal models.

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Growth factor protects key brain cells in Alzheimer's models

Memory loss, cognitive impairment, brain cell degeneration and cell death were prevented or reversed in several animal models after treatment with a naturally occurring protein called brain-derived neurotrophic factor (BDNF). The study by a University of California, San Diego-led team – published in the February 8, 2009 issue of Nature Medicine – shows that BDNF treatment can potentially provide long-lasting protection by slowing, or even stopping the progression of Alzheimer's disease in animal models. "The effects of BDNF were potent," said Mark Tuszynski, MD, PhD, professor of neurosciences at the UC San Diego School of Medicine and neurologist at the Veterans Affairs San Diego Health System. "When we administered BDNF to memory circuits in the brain, we directly stimulated their activity and prevented cell death from the underlying disease." BDNF is normally produced throughout life in the entorhinal cortex, a portion of the brain that supports memory. Its production decreases in the presence of Alzheimer's disease. For these experiments, the researchers injected the BDNF gene or protein in a series of cell culture and animal models, including transgenic mouse models of Alzheimer's disease; aged rats; rats with induced damage to the entorhinal cortex; aged rhesus monkeys, and monkeys with entorhinal cortex damage. In each case, when compared with control groups not treated with BDNF, the treated animals demonstrated significant improvement in the performance of a variety of learning and memory tests. Notably, the brains of the treated animals also exhibited restored BDNF gene expression, enhanced cell size, improved cell signaling, and activation of function in neurons that would otherwise have degenerated, compared to untreated animals. These benefits extended to the degenerating hippocampus where short-term memory is processed, one of the first regions of the brain to suffer damage in Alzheimer's disease.

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MRI shows brain atrophy pattern that predicts Alzheimer's

Using special MRI methods, researchers have identified a pattern of regional brain atrophy in patients with mild cognitive impairment (MCI) that indicates a greater likelihood of progression to Alzheimer's disease. The findings are published in the online edition of Radiology. "Previously, this pattern has been observed only after a diagnosis of probable Alzheimer's disease," said the study's lead author, Linda K. McEvoy, Ph.D., assistant project scientist in the Department of Radiology at the University of California San Diego School of Medicine in La Jolla. "Our results show that some individuals with MCI have the atrophy pattern characteristic of mild Alzheimer's disease, and these people are at higher risk of experiencing a faster rate of brain degeneration and a faster decline to dementia than individuals with MCI who do not show that atrophy pattern."According to the Alzheimer's Association, more than five million Americans currently have Alzheimer's disease. One of the goals of modern neuroimaging is to help in early and accurate diagnosis, which can be challenging. There is no cure for Alzheimer's disease, but when it is diagnosed early, drug treatment may help improve or stabilize patient symptoms. In Alzheimer's disease, nerve cell death and tissue loss cause areas of the brain to atrophy. Structural MRI allows radiologists to visualize subtle anatomic changes in the brain that signal atrophy. MCI is associated with an increased risk of progression to Alzheimer's disease. Rates of progression vary. Some patients progress rapidly, while others remain stable for relatively long periods of time.

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Alzheimer’s Toxin Identified

Researchers at UC Santa Barbara and other institutions have found evidence that a certain cluster of peptides--short chains of amino acids linked together--may be a toxic agent producing Alzheimer’s disease.

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Trigger for Alzheimer's identified

A new study by the Buck Institute for Age Research in Novato provides insight into the cause of Alzheimer's disease and suggests it may be possible to short-circuit the molecular mechanism that underlies it.

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New method to stimulate immune system may be effective at reducing amyloid burden in Alzheimer’s

Researchers at NYU Langone Medical Center have discovered a novel way to stimulate the innate immune system of mice with Alzheimer's disease (AD) - leading to reduced amyloid deposits and the prevention of Alzheimer's disease related pathology - without causing toxic side effects. The study entitled "Induction of Toll-like Receptor 9 Signaling as a Method for Ameliorating Alzheimer's Disease Related Pathology" was published in The Journal of Neuroscience. NYU Langone researchers stimulated the innate immune system via the Toll-like 9 receptor (TLR9) via treatment with cytosine-guanosine containing DNA oligodeoxynucleotides (CpG ODNs) in Tg2576 AD model transgenic mice. This treatment produced a 66% and 80% reduction in the cortical and vascular amyloid burden, when compared with non-treated AD mice. Also, vaccinated Tg2576 mice performed similarly to non-treated mice on a radial arm maze used in the study, showing improvements in behavior and reduced amyloid burden. "Our results indicate that stimulation of the innate immune system through TLR9 with CpG ODNs is an effective and apparently non-toxic method to reduce the amyloid burden in the brain," said Thomas Wisniewski, MD, professor of neurology, pathology and psychiatry at NYU Langone Medical Center. "Furthermore we found that amyloid reduction was associated with significant cognitive benefits in an AD mouse model. This approach has significant implications for future human immunomodulatory approaches to prevent AD in humans." The deposition of amyloid ? (A?) in the central nervous system in the form of amyloid plaques is a hallmark of Alzheimer's disease. A? accumulation destroys neurons in the brain, leading to deficits in cognitive abilities. Immunomodulation or vaccination for AD is emerging as an effective means of shifting the equilibrium from A? accumulation to clearance; however, excessive cell mediated inflammation and cerebral microhemorrhages - two forms of toxicity- were shown to occur in previous vaccination studies targeting the adaptive immune system.

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Rogue protein 'spreads in brain'

Scientists have shown a rogue protein thought to cause Alzheimer's can spread through the brain, turning healthy tissue bad.

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Alzheimer defect can be 'passed from one brain to another'

HARMFUL "tangles" of protein linked to Alzheimer's disease can be transmitted from one brain to another, scientists have discovered.

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Researchers use light to detect Alzheimer's

A team of researchers in Bedford, Mass. has developed a way of examining brain tissue with near-infrared light to detect signs of Alzheimer's disease.

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New study provides insight into ways organ systems outside the brain may affect Alzheimer's disease

In Alzheimer's disease the brain accumulates a molecule called A-beta that can be quite toxic to brain cells. Many researchers believe that finding ways to clear A-beta may be a key to treatment or prevention of Alzheimer's disease. A study published in the February issue of the Journal of Alzheimer's Disease provides new insights into the way A-beta in the peripheral blood stream affects A-beta clearance in the brain. Scientists from the University of Washington in Seattle, VA Puget Sound Health Care System, and the University of Hong Kong found that when circulating A-beta levels in the blood stream of rats were elevated, known amounts of radioactively tagged A-beta were swept from the brain more slowly. These findings directly demonstrate something researchers have proposed for several years now—that freely circulating A-beta concentrations outside the brain can regulate A-beta clearance rates inside the central nervous system. Researchers are coming to appreciate that the brain does not act alone in the task of clearing A-beta . It can be shuttled back and forth between compartments inside the brain and the peripheral blood supply where A-beta interacts with other organ systems. Treatments that increase the flow of A-beta away from the brain hold great therapeutic promise. Despite the promise of such work many basic questions still need to be answered about how the brain interacts with the rest of body to hold A-beta in check.

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Gladstone scientists find potential strategy to eliminate poisonous protein from Alzheimer brains

Scientists at the Gladstone Institute of Neurological Disease (GIND) have identified a new strategy to destroy amyloid-beta (AB) proteins, which are widely believed to cause Alzheimer's disease (AD). Li Gan, PhD, and her coworkers discovered that the activity of a potent AB-degrading enzyme can be unleashed in mouse models of the disease by reducing its natural inhibitor cystatin C (CysC). All of us produce AB proteins in the brain. However, in most people, the proteins never build up to dangerous levels because they are cleared away by enzymes that destroy them. Previously Dr. Gan's laboratory had shown that cathepsin B (CatB) is such an AB-degrading enzyme. In the latest issue of the journal Neuron, the researchers report a highly effective approach to promote CatB-mediated clearance of AB . "Many groups have developed drugs to block the production of AB, but the efficacy and safety of this approach remains to be demonstrated in clinical trials," said GIND Director Lennart Mucke, MD "By identifying an effective strategy to enhance the removal of AB, this research provides a very promising alternative or complementary therapeutic avenue." High levels of AB in the brain may result from overproduction of AB or from an inability to eliminate it from the brain. While most work has focused on the first option, the latter has been problematic. For example, efforts to develop a vaccine that would trigger the immune system to eliminate AB have shown limited success and resulted in adverse side effects. "Our strategy to harness the activity of a powerful AB-degrading enzyme takes advantage of the brain's own defense system to remove the toxic AB build-up," said Dr. Gan. "In principle, one could boost the activity of CatB by expressing more of it in the brain or by reducing the activity of CysC, its natural inhibitor. We focused on the latter strategy because it has greater long-term therapeutic potential." Many enzymes that degrade proteins are kept in check by regulators called protease inhibitors. The activity of CatB is regulated by the protease inhibitor CysC. By reducing CysC activity, the scientists were able to unleash the AB-degrading power of CatB, effectively preventing the build-up of AB in mouse models of AD.

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Inflammation may trigger Alzheimer's disease, Saint Louis University findings suggest

The anti-inflammatory drug indomethacin could hold promise as a treatment for Alzheimer's disease, says a Saint Louis University doctor and researcher. Two research studies published by William A. Banks, M.D., professor of geriatrics and pharmacological and physiological science at Saint Louis University School of Medicine, support this conclusion and offer what he calls a "one-two punch" in giving clues on how Alzheimer's disease develops and could be treated. His study in the July edition of the Journal of Alzheimer's Disease supports the idea that toxic levels of amyloid beta protein, the substance scientists believe is responsible for Alzheimer's disease, accumulate in the brain because a pump that pushes it into the blood and past the blood-brain barrier malfunctions. The blood-brain barrier is a system of cells that regulates the exchange of substances between the brain and the blood. The blood-brain barrier transporter known as LRP is the pump that removes amyloid beta protein from the brain and into the bloodstream. "LRP malfunctions like a stop light stuck on red, and keeps amyloid beta protein trapped in the brain," said Banks, who also is a staff physician at Veterans Affairs Medical Center in St. Louis. He tested the hypothesis by giving mice an antisense, which is a molecular compound that blocked the production of LRP. Amyloid beta protein accumulated in the brain and the mice showed memory loss and learning impairment. The finding raises the question of what causes LRP to malfunction. Banks' study in the May issue of Brain Behavior and Immunity suggests inflammation as the culprit and supports using indomethacin, an anti-inflammatory medication, as a buffer to protect LRP from being turned off. Inflammation, which is part of the body's natural immune response, occurs when the body activates white blood cells and produces chemicals to fight infection and invading foreign substances.

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Forgotten and lost - when proteins "shut down" our brain

Which modules of the tau protein, in neurons of Alzheimer disease patients, may act in a destructive manner were investigated by researchers from the Max Planck Institute for Biophysical Chemistry (GŲttingen) and the Max Planck Unit for Structural Molecular Biology (Hamburg) with the help of Nuclear Magnetic Resonance Spectroscopy (PLoS Biology, February 17, 2009). Coordination becomes difficult, items disappear, keeping new information in the mind is impossible. Worldwide almost 30 million people suffer from Alzheimer’s disease, a neurodegenerative, irreversible ailment which starts with memory gaps and ends in helplessness and the loss of personality. The most critical factor in developing Alzheimer’s disease is age. Most cases occur after the age of 65. Two hallmarks are typical for Alzheimer affected brains. One of them, located between nerve cells, is amyloid plaques - extracellular protein aggregates mainly composed of a protein named beta-amyloid. The other clue is intracellular tau fibrils. In the interplay with genetic factors, the latter contribute to a disordered communication within the cell. This triggers cell death. But the tau protein is not only harmful. Quite the contrary is the case. In its normal non-pathogenic form tau binds to microtubules, long tubular cytoskeletal building blocks, which serve as "tracks" for intracellular transport. In patients afflicted by Alzheimer’s disease or similar dementia, tau is abnormally altered. In its pathogenic form tau possesses more phosphorylated amino acids than in its normal healthy counterpart. "Our interest was focussed on how certain phosphorylated residues alter the structure of tau in a way that it can not bind to microtubules anymore" explains Markus Zweckstetter at the Max Planck Institute for Biophysical Chemistry.

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Most neuropsychological tests don't tell Alzheimer's disease from vascular dementia

Most of the cognitive tests that have been used to decide whether someone has Alzheimer's disease or vascular dementia have not been very helpful when used alone. A new report published by the American Psychological Association concluded that when older people are confused and forgetful, doctors should base their diagnoses on many different types of information, including medical history and brain imaging. Both Alzheimer's disease and vascular dementia affect learning and memory, behavior and day-to-day function. Even so, they're caused by different problems in the brain and require different medical approaches. It's important to tell them apart accurately, stresses the study in July's Neuropsychology. Valid diagnoses can help doctors treat patients more effectively, and help patients and families better understand their situations. Jane Mathias, PhD, and Jennifer Burke, M.Psych.(Clinical), both from the University of Adelaide, analyzed 81 previously published studies that compared the cognitive testing of people diagnosed with dementia of the Alzheimer's (4,867) and vascular type (2,263). The average age across participants was 75. Of the 118 different tests that were used in more than one study, Mathias and Burke found that only two were able to adequately differentiate between Alzheimer's and vascular dementia. The Emotional Recognition Task (the ability to identify facial expressions in photographs and match emotional expressions to situations, at which people with Alzheimer's were better) and Delayed Story Recall (at which people with vascular dementia were better), were the only tests that appeared to reliably tell the two groups apart.

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Ground-breaking Alzheimer's findings reveal new treatment strategy

Alzheimer’s disease affects the major two types of brain cells, neurones and neuroglia. For a long time glial cells have been thought to have a purely supportive role. However, recent work and more specifically ongoing studies at the University of Manchester are probing a much more relevant functional role including new treatment opportunities, for neurodegenerative processes such as Alzheimer’s disease. Dr Josť J. RodrŪguez Arellano and Professor Alexei Verkhratsky believe that, contrary to popular belief, neuroglial cells (astrocytes) in the brain shrink during Alzheimer’s disease. Astrocytes are vital in providing for generation and maintenance of synapses and therefore diminished astroglial support alters synaptic connectivity thus redusing brain cognitive power. They say that probably the new strategies aimed at protection and support of neuroglia may help to combat brain degeneration in Alzheimer disease. Dr Rodriguez-Arellano, whose work was funded by the Alzheimer’s Research Trust, says: “These are amazing findings and totally unexpected. We have found that model animals (transgenic mice) with Alzheimer’s pathology have problems with glial cells as well as with the neurones in the brain. “Everybody thought that glial cells grew bigger in response to the disease but we have found that some of them actually shrink and this causes serious problems. Glial cells are not merely supportive; they have an active role in maintaining synapses so the imbalance of these cells can have a serious negative effect.”

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Researchers surprised by similar structures in Sanfilippo syndrome and Alzheimer's disease

Researchers seeking to understand the causes of a rare genetic lysosomal storage disease, Sanfilippo syndrome type B, were surprised to find protein aggregates, known as neurofibrillary tangles, that are usually seen in Alzheimer's and other forms of dementia, according to a study published May 4 in the Proceedings of the National Academy of Sciences. The discovery, in a study conducted at the Los Angeles Biomedical Research Institute (LA BioMed) and the University of California, Los Angeles (UCLA), means that the childhood dementia often seen in lysosomal storage diseases may have mechanisms similar to those found in Alzheimer's disease and other age-related dementias, which are characterized by an abnormal accumulation of the protein, P-tau. The scientists also said these findings mean those suffering from these rare disorders could one day benefit from the abundance of research underway for the growing numbers of Alzheimer's patients.

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Increased level of magnetic iron oxides found in Alzheimer's disease

A team of scientists, led by Professor Jon Dobson, of Keele University in Staffordshire, UK, have found, for the first time, raised levels of magnetic iron oxides in the part of the brain affected by Alzheimer's Disease. The results of their research have been published in the Journal of Alzheimer's Disease

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GPS Shoes - Tracking Parents With Alzheimer's Disease

a designer of orthopedic footwear and a GPS tracking manufacturer have just announced an agreement to develop GPS-embedded orthopedic footwear for seniors with dementia. Aetrexģ and GTX™ corporations formed their partnership to enable loved ones and caretakers to know where the Alzheimer's patient is at all times, with almost-certainty that his or her shoes will not be removed.

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How neuronal activity leads to Alzheimer's protein cleavage

Amyloid precursor protein, whose cleavage product, amyloid-b, builds up into fibrous plaques in the brains of Alzheimer's disease patients, jumps from one specialized membrane microdomain to another to be cleaved, report Sakurai et al in the Journal of Cell Biology.

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Discovery of brain protein may be clue to treatment

A study from the Buck Institute for Age Research offers a revolutionary new model for Alzheimer’s disease (AD), a devastating neurodegenerative disorder which afflicts 24 million people worldwide. In an effort to unravel the normal function of a protein implicated in AD, scientists in California and France have discovered a naturally occurring protein that provides a new therapeutic target for the disease. The finding upsets the current theory that AD is a disease of toxicity stemming from damage caused by sticky plaques that collect in the brain – this research points to the condition as a disorder involving an imbalance in signaling between neurons. The study appears online in the Nature publication Cell Death and Differentiation. One of the mysteries of AD has been the normal function of the amyloid precursor protein (APP) which are concentrated at the points where neurons connect. Even though the sticky amyloid plaques which have been viewed as a hallmark sign of AD result from APP, it seems unlikely that APP exists simply to cause Alzheimer’s disease. In their study, scientists from the Buck Institute and the CNRS (Centre Nationale de la Recherche Scientifique) show that APP binds to netrin-1, a protein that helps to guide nerves and their connections in the brain, as well as helping nerve cells to survive. When netrin-1 was given to mice that have a gene for Alzheimer’s disease their symptoms were reversed, and the sticky amyloid was reduced. These results suggest that the long-held belief that AD is caused by brain cell damage inflicted by the amyloid plaques may be wrong; instead, it is beginning to appear that the disease stems from an imbalance between the normal making and breaking of connections in the brain, with netrin-1 supporting the connections and the amyloid breaking the connections -- both by binding to APP and activating normal cell programs. Not only did the netrin-1 binding to APP keep the nerve cells alive and connected, but it also shut down the production of the amyloid, all of which makes it an interesting potential therapeutic.

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Radiologists identify early brain marker of Alzheimer's disease

Researchers using functional magnetic resonance imaging have found a new marker which may aid in early diagnosis of Alzheimer's disease, according to a study published in the October issue of Radiology.

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Gladstone scientists identify role of fatty acids in Alzheimer's disease

Scientists at the Gladstone Institute of Neurological Disease and the University of California have found that complete or partial removal of an enzyme that regulates fatty acid levels improves cognitive deficits in a mouse model of Alzheimer's disease.

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A high-fat diet could promote the development of Alzheimer's

A team of Universitť Laval researchers has shown that the main neurological markers for Alzheimer's disease are exacerbated in the brains of mice fed a diet rich in animal fat and poor in omega-3s. Details of the study—which suggests that diets typical of most industrialized countries promote the development of Alzheimer's—are outlined in the latest online edition of Neurobiology of Aging. To demonstrate this, the team led by Frťdťric Calon used a type of transgenic mice that produce two proteins found in the brains of Alzheimer patients—tau proteins, which prevent proper neuron functioning, and amyloid-beta, associated with the formation of senile plaques within the brains of afflicted patients. The researchers fed transgenic and regular mice different diets for nine months, after which they compared the effects on the animals' brains. The mice whose diet was poor in omega-3s and rich in fat (60% of consumed calories) showed amyloid-beta and tau protein concentrations respectively 8.7 and 1.5 times higher than the control group mice, whose food contained 7 times less fat. The high-fat diet also reduced drebrin protein levels in the brain, another characteristic of Alzheimer's disease. "Metabolic changes induced by such a diet could affect the inflammatory response in the brain," suggests study co-author Carl Julien to explain the link between fat consumption and Alzheimer's. In most Western countries, diets rich in saturated fats and poor in omega-3s are the norm. "Our findings lead us to believe that a diet containing more omega-3s and less saturated fat could prevent the development of Alzheimer's, at the very least among people genetically predisposed to the disease," comments Dr. Calon. "We cannot state with any certainty that what we have observed among transgenic mice also occurs in humans, but there is no harm in eating less fat and more omega-3s," concludes the researcher.

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Mount Sinai researchers find new Alzheimer's disease treatment promising

Researchers at Mount Sinai School of Medicine have found that a compound called NIC5-15, might be a safe and effective treatment to stabilize cognitive performance in patients with mild to moderate Alzheimer's disease. The two investigators, Giulio Maria Pasinetti, M.D., Ph.D. , and Hillel Grossman, M.D., presented Phase IIA preliminary clinical findings at the Alzheimer's Association 2009 International Conference on Alzheimer's Disease (ICAD) in Vienna on Sunday, July 12. NIC5-15's potential to preserve cognitive performance will be further evaluated in a Phase IIB clinical trial. Early evidence suggests that NIC5-15 is a safe and tolerable natural compound that may reduce the progression of Alzheimer's disease-related dementia by preventing the formation of beta-amyloid plaque, a waxy substance that accumulates between brain cells and impacts cognitive function. "With Alzheimer's disease affecting 5.2 million Americans, another 5 million with early-state disease, and nearly a half million new cases reported annually, treatments like NIC5-15 would make a significant difference in the lives of many Alzheimer's patients," said Dr. Pasinetti, Professor of Psychiatry, Professor of Neuroscience and Professor of Geriatrics and Adult Development, in the Department of Psychiatry at Mount Sinai School of Medicine. "We are hopeful that the follow up clinical study will support this preliminary evidence."

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Results from trials of DHA in Alzheimer's disease and age-related cognitive decline

Results from two large studies using DHA, an omega 3 fatty acid, were reported today at the Alzheimer's Association 2009 International Conference on Alzheimer's Disease (ICAD 2009) in Vienna. One of the trials was conducted by the Alzheimer's Disease Cooperative Study (ADCS) supported by the National Institute on Aging (NIA), and the second by Martek Biosciences Corporation (Martek), the primary company that makes algal DHA for supplementation. The NIA trial lasted 18 months and was conducted in people with mild to moderate Alzheimer's. Martek's trial was six months, and the compound was tested in healthy people to see its effect on "age related cognitive decline" (ARCD). Both studies used Martek's algal DHA. The results of the ADCS trial show no evidence for benefit in the studied population. The Martek trial showed a positive result on one test of memory and learning, but that study was in healthy older adults, not people with Alzheimer's or another dementia. The results need confirmation, as is standard scientific practice. "These two studies – and other recent Alzheimer's therapy trials – raise the possibility that treatments for Alzheimer's must be given very early in the disease for them to be truly effective," said William Thies, PhD, Chief Medical & Scientific Officer at the Alzheimer's Association. "For that to happen, we need to get much better at early detection and diagnosis of Alzheimer's, in order to test therapies at earlier stages of the disease and enable earlier intervention." Other research studies from ICAD 2009 show advances made in biomarkers and early detection from the Alzheimer's Disease Neuroimaging Initiative (ADNI), and also survey results from doctors about the enablers and barriers they face in diagnosing people with Alzheimer's. DHA (docosahexaenoic acid) is naturally found in the body in small amounts, and is the most abundant omega 3 fatty acid in the brain. DHA oil is abundant in some marine microalgae, which provide the DHA that makes fatty fish a good source of DHA. Dietary DHA is also available in foods enriched with algal DHA or fish oils, and dietary supplements. Previous animal studies and epidemiology in humans suggested that DHA may be beneficial in people with Alzheimer's.

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New evidence ties gene to Alzheimer's

Of dozens of candidates potentially involved in increasing a person's risk for the most common type of Alzheimer's disease that affects more than 5 million Americans over the age of 65, one gene that keeps grabbing Johns Hopkins researchers' attention makes a protein called neuroglobin. Adding to a growing body of evidence about the importance of this protein for the health of the aging brain, researchers at the McKusick-Nathans Institute of Genetic Medicine of the Johns Hopkins University School of Medicine canvassed the genetic neighborhood of neuroglobin and, for the first time in a human population, linked variation there with a risk for Alzheimer's. Ever so slight genetic variations between individuals can and do influence the amounts of particular proteins that each specific gene ultimately produces. In this case, the team has found that individuals with genetic variations equating to less neuroglobin production have an increased risk for Alzheimer's. "An intriguing part of this study was the high levels of neuroglobin that we found in the Alzheimer's brain, which was exactly the opposite from what we expected," says Dimitrios Avramopoulos, M.D., Ph.D., an associate professor in Hopkins' Institute of Genetic Medicine and the Department of Psychiatry. Referring to data published in Neurobiology of Aging, Avramopoulos explains that his team measured levels of gene product in 56 different samples of human brain tissue: 30 from confirmed cases of Alzheimer's and 26 without brain disease. The scientists found that neuroglobin levels decreased with advancing age, which, Avramopoulos points out, is consistent with risk of Alzheimer's increasing with advancing age. They also found that levels of neuroglobin were lower in women than in men, which is consistent with the fact that women have a slightly higher risk of Alzheimer's. About two times as many patients in the general population with Alzheimer's are women which, in part, can be attributed to the fact that women live longer and therefore have more of a chance to get Alzheimer's. Having corrected for that disparity, researchers have noted a slightly higher risk in women than in men. They were surprised to find that neuroglobin levels were higher in the brain tissue from Alzheimer's patients than that of the control group.

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Mechanisms that prevent Alzheimer's Disease

In a project involving the collaboration of several institutes, research scientists of the Johannes Gutenberg University Mainz have succeeded in gaining further insight in the functioning of endogenous mechanisms that protect against the development of Alzheimer's disease. It was found that the activity of the enzyme ?-secretase is mainly responsible for the protective effect. "In the past, we postulated that the enzyme ?-secretase was involved in preventing the formation of cerebral plaques characteristic of Alzheimer's disease and also enhanced cerebral functions, such as learning and memory," explained Professor Falk Fahrenholz of the Institute of Biochemistry. His research group has been working in cooperation with the Clinic of Psychiatry and Psychotherapy of the university's Faculty of Medicine and the Central Animal Laboratory Facility (ZVTE) to discover the mechanism for the beneficial effects of ?-secretase. The Journal of Alzheimer's Disease (JAD) presents the results of this project in its February 2009 issue. ?-secretase is an endogenous enzyme that is present in the nerve cells of the brain, where it is responsible for the cleavage of an A? into A? domain. The result is a soluble protein fragment that promotes the growth of nerve cells and thus prevents the development of cerebral deterioration caused by A?. However, if the enzyme ?-secretase is active, a chain reaction is initiated that subsequently results in the development A? initializing the cascade of Alzheimer's disease through formation of A?. "You could say that ?-secretase is the good enzyme, and ?-secretase the bad en-zyme," Fahrenholz commented. "We now want to find out how to activate this 'good' enzyme or increase its concentrations in the brain as a way of combating this disease."

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Fresh theory on Alzheimer's

CHEMICALS found in many fruits and vegetables, as well as tea, cocoa and red wine, could protect the brain from Alzheimer's disease, a conference in Edinburgh heard today.

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UCLA scientists identify how immune cells may help predict Alzheimer's risk

What if you could test your risk for Alzheimer's disease much like your cholesterol levels — through a simple blood test? UCLA scientists have discovered a way to measure the amount of amyloid beta that is being absorbed by immune cells in the blood. Amyloid beta forms the plaques considered the hallmark of Alzheimer's disease, and if the immune system isn't adequately clearing amyloid beta, it may indicate Alzheimer's risk, according to the researchers. MP Biomedicals LLC, a global life sciences and diagnostics company dedicated to Alzheimer's disease research, has received an exclusive, worldwide license to commercialize the UCLA technology and create a diagnostic blood test for public use to screen for Alzheimer's risk. "Early diagnosis is the cornerstone of preventive approaches to Alzheimer's disease," said Dr. Milan Fiala, lead author of the UCLA study and a researcher at the David Geffen School of Medicine at UCLA and the Veterans Affairs Greater Los Angeles Healthcare System. "We are pleased that the process we've identified using immune cells to help predict Alzheimer's risk will be further developed by MP Biomedicals." "We are excited by the opportunity to forward the UCLA science in creating a cost-effective blood test to screen for Alzheimer's risk that could be used in any hospital or lab," said Milan Panic, CEO of MP Biomedicals. Dr. Miodrag Micic, vice president of research and development for MP Biomedicals, noted that other blood tests for Alzheimer's diagnosis measure factors such as inflammation and infection, which are also present in other diseases like atheroclerosis and may complicate the interpretation of results.

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New brain marker shows promise for predicting future Alzheimer's disease

Duke University Medical Center researchers have used imaging technology to identify a new marker that may help identify those at greatest risk for cognitive decline and the development of Alzheimer's disease.

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Gene scan of Alzheimer’s families identifies four new suspect genes

The first family-based genome-wide association study in Alzheimer’s disease has identified the sites of four novel genes that may significantly influence risk for the most common late-onset form of the devastating neurological disorder. In their report in the November 7 American Journal of Human Genetics, being released online today, a team led by researchers from the MassGeneral Institute for Neurodegenerative Disease (MGH-MIND) describes how newly available technology is improving understanding of genetic mechanisms underlying the disease. The study presents the first results of the Alzheimer’s Genome Project supported by the Cure Alzheimer’s Fund and the National Institute of Mental Health.

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No benefit found from continuing neuroleptic drugs in Alzheimer's patients

Results of a randomized trial published in PLoS Medicine show no benefit in cognitive or neuropsychiatric outcomes from continuing neuroleptic drugs in patients with Alzheimer's disease.

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Research links diet to cognitive decline and dementia

Research has shown convincing evidence that dietary patterns practiced during adulthood are important contributors to age-related cognitive decline and dementia risk.

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A 'grape' future for Alzheimer's disease research

Research with grape polyphenols presented today at Neuroscience 2007 in San Diego shows promise for maintaining long-term cognitive health. The researchers will now focus on grape polyphenols and Alzheimer's disease at the newly established Center for Research in Alternative and Complementary Medicine in Alzheimer's disease research at Mount Sinai School of Medicine.

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A Randomised, Blinded, Placebo-Controlled Trial in Dementia Patients Continuing or Stopping Neuroleptics

For most patients with AD, withdrawal of neuroleptics had no overall detrimental effect on functional and cognitive status and by some measures improved functional and cognitive status. Neuroleptics may have some value in the maintenance treatment of more severe neuropsychiatric symptoms, but this possibility must be weighed against the unwanted effects of therapy. The current study helps to inform a clinical management strategy for current practice, but the considerable risks of maintenance therapy highlight the urgency of further work to find, develop, and implement safer and more effective treatment approaches for neuropsychiatric symptoms in people with AD.

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Mitochondria play role in pathogenesis of AD and estrogen-induced neuroprotection

As the major source of free radicals in cells, mitochondria contribute to the high levels of oxidative stress believed to play a role in the pathogenesis of Alzheimer's disease. Now a study demonstrates that estrogen reduces this oxidative stress caused by the mitochondria while increasing the ability of the mitochondria to generate energy -- important since there is usually an energy deficit in the Alzheimer brain.

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Lilly Touted Zyprexa for Alzheimer's Knowing It Was Ineffective

Eli Lilly knew in 1995 that Zyprexa was ineffective for treating Alzheimer’s and dementia in the elderly but promoted it for that purpose anyway, according to a lawsuit. The suit also claims that each Zyprexa sales rep had a $10,000 budget that it used to pay pharmacies and doctors for talking up off-label uses of Zyprexa.

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Aluminum, silica in water affect Alzheimer's risk

Higher levels of aluminum in drinking water appear to increase people's risk of developing Alzheimer's disease, whereas higher levels of silica appear to decrease the risk, according to French investigators.

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Divorce triples your risk of Alzheimer's

If you’re middle-aged, get divorced and live alone, you triple your chances of Alzheimer’s according to research that looked at the brain health of more than 2,000 Finns.

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Mortality With Antipsychotic Use in Alzheimer Disease

Mortality in elderly patients with dementia markedly and progressively increases with extended use of antipsychotics, according to the first long-term controlled study of risk in this population. Earlier evidence of this risk was from short-term trials not exceeding 14 weeks.

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Mitochondria Could Be a Target for Therapeutic Strategy for Alzheimer’s Disease Patients

A study in the edition of Nature Medicine describes the function and interaction of a critical molecule involved in cell death in Alzheimer’s disease patients. These new findings reveal that blocking this molecule, called Cyclophilin D (CypD), and development of surrounding mitochondrial targets may be viable therapeutic strategies for the prevention and treatment of Alzheimer’s disease, according to Shi Du Yan, Ph.D., professor of clinical pathology in the Department's of Pathology and Surgery and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University Medical Center, who led the multi-center research. This paper strengthens the concept that mitochondrial permeability pores may be central in mitochondrial and neuronal malfunction relevant to Alzheimer disease. Dr. Yan and her colleagues offer new insights into the mechanism underlying amyloid beta (A?)-mediated mitochondrial stress through an interaction with CypD, which is linked to synaptic plasticity and learning/memory. Importantly, these findings may help explain the mechanism of action of a medication already in use in clinical trials.

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Protecting neurons could halt Alzheimer's, Parkinson's diseases

Researchers at Southern Methodist University (SMU) and The University of Texas at Dallas (UTD) have identified a group of chemical compounds that slow the degeneration of neurons, a condition behind old-age diseases like Alzheimer's, Parkinson's and amyotrophic lateral sclerosis (ALS). Their findings are featured in the November 2008 edition of Experimental Biology and Medicine. SMU Chemistry Professor Edward R. Biehl and UTD Biology Professor Santosh D'Mello teamed to test 45 chemical compounds. Four were found to be the most potent protectors of neurons, the cells that are core components of the human brain, spinal cord and peripheral nerves.The most common cause of neurodegenerative disease is aging. Current medications only alleviate the symptoms but do not affect the underlying cause – degeneration of neurons. The identification of compounds that inhibit neuronal death is of urgent and critical importance.

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Dietary acrylamide may play a role in Alzheimer’s, researchers theorize

Scientists have known for years that acrylamide is capable of causing nerve damage in humans, including muscle weakness and impaired muscle coordination, particularly from industrial exposure to large levels of the chemical. Now, new laboratory studies suggest that chronic dietary exposure to the chemical is capable of damaging nerve cells in the brain and could potentially play a role in the development of neurodegenerative disease, including Alzheimer’s, according to Richard LoPachin, Jr., Ph.D., a neurotoxicologist with Albert Einstein College of Medicine in New York. He notes that acrylamide is structurally similar to acrolein, a chemical found in increased levels in brains of patients with Alzheimer’s and other neurodegenerative diseases. Studies in humans are warranted, the researcher says.

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Discovery supports theory of Alzheimer's disease as form of diabetes

Insulin may be as important for the mind as it is for the body. Recent research has raised the possibility that Alzheimer's memory loss could be due to a novel third form of diabetes. Scientists at Northwestern University have discovered why brain insulin signaling would stop working in Alzheimer's disease. They have shown that a toxic protein found in the brains of individuals with Alzheimer's removes insulin receptors from nerve cells, rendering those neurons insulin-resistant.

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Vitamin 'may be Alzheimer's aid'

A vitamin found in meat, fish and potatoes may help protect the brain from Alzheimer's disease - and even boost memory in healthy people.US researchers found vitamin B3 lowered levels of a protein linked to Alzheimer's damage in mice.

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Redox-active iron is a sensor of cognitive impairment associated with Alzheimer's disease

An innovative discovery has been reported that highlights the problems that oxidative stress resulting from iron cumulated in the human brain can generate in relation with the pathogenesis of Alzheimer's disease, the brain disorder affecting almost 30 million throughout the world. The results of research appeared recently in Volume 13, Issue 2 of the prestigious Journal of Alzheimer's Disease.

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A special type of collagen may help protect the brain against Alzheimer's disease

Scientists from the Gladstone Institute of Neurological Disease (GIND), UCSF, and Stanford have discovered that a certain type of collagen, collagen VI, protects brain cells against amyloid-beta (A? ) proteins, which are widely thought to cause Alzheimer's disease (AD). While the functions of collagens in cartilage and muscle are well established, before this study it was unknown that collagen VI is made by neurons in the brain and that it can fulfill important neuroprotective functions. The team of investigators led by GIND director Lennart Mucke, MD, reported in a recent edition of the journal Nature Neuroscience, that collagen VI is increased in brain tissues of Alzheimer's patients. "We first noticed the increase in collagen VI in the brain of AD mouse models, which inspired us to look for it in the human condition and to define its role in the disease," said Dr. Mucke. The Gladstone team had profiled changes in gene expression using DNA microarrays, which provides an unbiased method for identifying key biological pathways. By comparing all of the genes that are active in disease and normal tissue, one can get valuable information on new pathways and potential therapeutic targets. The researchers looked at the dentate gyrus, a specific area of the brain that is critical to memory and particularly vulnerable in AD, and compared the genes that were turned on and off in normal mice and a mouse model of AD. This analysis revealed the striking increase in collagen VI in the brains of mice that model AD. Building on this initial finding, the team examined brain tissue from AD patients and normal non-demented humans and found that collagen VI expression was also higher in the AD patients. They further discovered that the cellular source of the collagen VI in the brain was neurons, the very cells that the disease attacks and that we all need to think and remember.

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Alzheimer's molecule is a smart speed bump on the nerve-cell transport highway

Researchers at the University of Pennsylvania School of Medicine discovered that proteins carrying chemical cargo in nerve cells react differently when exposed to the tau protein, which plays an important role in Alzheimer's disease.

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Evidence found for genes that affect risk of developing Alzheimer's disease

Through one of the largest studies yet of Alzheimer's disease patients and their brothers, sisters, and children, researchers at Mayo Clinic Jacksonville have found strong evidence that genes other than the well-known susceptibility risk factor APOE4 influence who is at risk for developing the neurodegenerative disease later in life.

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Altering brain's lipid metabolism reduces Alzheimer's plaques in mice

Increasing levels of a protein that helps the brain use cholesterol may slow the development of Alzheimer's disease changes in the brain, according to researchers studying a mouse model of the disease at Washington University School of Medicine in St. Louis.

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Alzheimer’s disease breakthrough

In a paper published in the latest edition of the Journal of Alzheimer’s Disease, folate is shown to be beneficial in the screening system. Lead author, CSIRO’s Dr Ian Macreadie says folate is already well known to have a protective effect against Alzheimer’s disease which is believed to be caused by the loss of neurons in the brain due to a process whereby toxic multimers of a small protein called A? are formed. “However, a team of scientists working within CSIRO’s Preventative Health Flagship has discovered a rapid screening system to identify inhibitors of this process. Compounds that inhibit the formation of the toxic multimers may lead to the prevention or delay of the disease,” Dr Macreadie says. “Although many other research groups and drug companies around the world are trying to find compounds that act in the same way, the advance by the Flagship team involves using live yeast with the A? protein fused to a green fluorescent protein that comes from jellyfish.

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UCF research links proteins, stem cells and potential Alzheimer's treatment

UCF researcher finds link between protein and stem cells, which may lead to a new way to treat Alzheimer's disease.

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Researchers link metal ions to neurodegenerative disease

Researchers have defined for the first time how metal ions bind to amyloid fibrils in the brain in a way that appears toxic to neurons. Amyloid fibrils are linked to the development of neurodegenerative diseases such as Alzheimer's, Parkinson's and Creutzfeldt-Jakob. Although metal ions, most notably copper, can bind to amyloid in several specific ways, the researchers found that only one way appears toxic.

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MRI brain scans accurate in early diagnosis of Alzheimer's disease

MRI scans that detect shrinkage in specific regions of the mid-brain attacked by Alzheimer’s disease accurately diagnose the neurodegenerative disease, even before symptoms interfere with daily function, a study by the Florida Alzheimer’s Disease Research Center (ADRC) in Miami and Tampa found. The study, reported earlier this month in the journal Neurology, adds to a growing body of evidence indicating MRI brain scans provide valuable diagnostic information about Alzheimer’s disease. The findings are important in light of many new disease-modifying drugs in trials -- treatments that may prevent mild memory loss from advancing to full-blown dementia if administered early enough. "We advocate, based on these findings, that the criteria for the diagnosis of Alzheimer’s disease should include MRI scans,” said the study’s lead author Ranjan Duara, MD, medical director of the Wien Center for Alzheimer’s Disease and Memory Disorders at Mount Sinai Medical Center who is affiliated with the University of Miami Miller School of Medicine and University of South Florida College of Medicine. “By incorporating MRIs into the assessment of patients with memory problems, early diagnosis can be standardized and done far more accurately.”

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Altering Brain's Lipid Metabolism Reduces Alzheimer's Plaques In Mice

Increasing levels of a protein that helps the brain use cholesterol may slow the development of Alzheimer's disease changes in the brain, according to researchers studying a mouse model of the disease at Washington University School of Medicine in St. Louis.

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Tel Aviv University researcher goes 'through the nose' to delay onset of Alzheimer's disease

Tel Aviv University researcher goes 'through the nose' to delay onset of Alzheimer's diseaseNew drug candidate dissolves plaques associated with Alzheimer's and other neurological diseases.

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Calpain inhibitors never forget - Improving memory in Alzheimer's disease mice

Overactivation of proteins known as calpains, which are involved in memory formation, has been linked to Alzheimer disease. Ottavio Arancio and colleagues, at Columbia University, New York, have now shown that two different drugs that inhibit calpains can improve memory in a mouse model of Alzheimer disease (APP/PS1 mice), leading them to suggest drugs that target calpains might stop or slow down the memory loss that occurs as Alzheimer disease progresses.It is thought that dysfunctional signaling between nerve cells contributes to the impaired cognition experienced by individuals with Alzheimer disease. In the study, analysis of cells and tissue slices from APP/PS1 mice, specifically cells from the part of the brain known as the hippocampus and hippocampal slices, indicated that exposure to calpain inhibitors restored signaling between nerve cells to normal. The authors therefore suggest that calpain inhibitors improve memory in APP/PS1 mice because they reestablish normal signaling between nerve cells.

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Two cardiovascular proteins pose a double whammy in Alzheimer's

Researchers have found that two proteins which work in tandem in the brain's blood vessels present a double whammy in Alzheimer's disease. Not only do the proteins lessen blood flow in the brain, but they also reduce the rate at which the brain is able to remove amyloid beta, the protein that builds up in toxic quantities in the brains of patients with the disease. The work, described in a paper published online Dec. 21 in the journal Nature Cell Biology, provides hard evidence directly linking two processes thought to be at play in Alzheimer's disease: reduction in blood flow and the buildup of toxic amyloid beta. The research makes the interaction between the two proteins a seductive target for researchers seeking to address both issues. Scientists were surprised at the finding, which puts two proteins known for their role in the cardiovascular system front and center in the development of Alzheimer's disease. "This is quite unexpected," said Berislav Zlokovic, M.D., Ph.D., a neuroscientist and a senior author of the study. "On the other hand, both of these processes are mediated by the smooth muscle cells along blood vessel walls, and we know that those are seriously compromised in patients with Alzheimer's disease, so perhaps we shouldn't be completely surprised." The new findings are the result of a seven-year collaboration between two laboratories. Zlokovic heads the Center for Neurodegenerative and Vascular Brain Disorders, looking at molecular roots of diseases like Alzheimer's. Several years ago, after he found that several genes well known to cardiovascular researchers seemed to be especially affected in Alzheimer's patients, he turned to Joseph Miano, Ph.D. to help analyze the findings. Miano is interim director of Aab Cardiovascular Research Institute and associate professor of Medicine, and he is senior co-author of the new study.

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Grapeseedextract as effective as red wine in preventing amyloid beta plaque build up

A compound found in grape seed extract reduces plaque formation and resulting cognitive impairment in an animal model of Alzheimer’s disease, new research shows. The study appears in the June 18 issue of The Journal of Neuroscience. Lead study author Giulio Pasinetti, MD, PhD, of Mount Sinai School of Medicine and colleagues found that the grape seed extract prevents amyloid beta accumulation in cells, suggesting that it may block the formation of plaques. In Alzheimer’s disease, amyloid beta accumulates to form toxic plaques that disrupt normal brain function. The researchers tested a grape seed polyphenolic extract product sold as MegaNatural-AZ, made by Polyphenolics, which in part supported the study. Polyphenolic compounds are antioxidants naturally found in wine, tea, chocolate, and some fruits and vegetables. To determine whether the extract could mitigate the effects of Alzheimer’s disease, the researchers used mice genetically modified to develop a condition similar to Alzheimer’s disease. They exposed pre-symptomatic “Alzheimer’s mice” to the extract or placebo daily for five months. The daily dose of the polyphenolic extract was equivalent to the average amount of polyphenolics consumed by a person on a daily basis.

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Brain starvation as we age appears to trigger Alzheimer's

A slow, chronic starvation of the brain as we age appears to be one of the major triggers of a biochemical process that causes some forms of Alzheimer's disease. A new study from Northwestern University's Feinberg School of Medicine has found when the brain doesn't get enough sugar glucose -- as might occur when cardiovascular disease restricts blood flow in arteries to the brain -- a process is launched that ultimately produces the sticky clumps of protein that appear to be a cause of Alzheimer's. Robert Vassar, lead author, discovered a key brain protein is altered when the brain has a deficient supply of energy. The altered protein, called elF2alpha, increases the production of an enzyme that, in turn, flips a switch to produce the sticky protein clumps. Vassar worked with human and mice brains in his research.

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Draining away brain's toxic protein to stop Alzheimer's

Scientists have shown how the body's natural way of ridding the body of the toxic protein amyloid-beta is flawed in people with the disease. Then the team demonstrated an experimental method in mice to fix the process, dramatically reducing the levels of the toxic protein in the brain and halting symptoms.

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Glaucoma could be early warning for Alzheimer's

Scientists at University College London (UCL) found a "clear link between what causes Alzheimer's and one of the basic mechanisms behind glaucoma".

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Mechanistic Link Discovered between Calcium Signaling and Alzheimer Gene

Scientists from the Institute for Aging and Alzheimer’s Disease Research (IAADR) based in Fort Worth, Texas, have discovered a molecular mechanism that links the activity of a crucial protein involved in Alzheimer’s disease with a fundamental signaling process in nerve cells. Published online in The International Journal of Biochemistry & Cell Biology , the research was funded by the National Institute on Aging (NIA), part of the National Institutes of Health (NIH) and the Alzheimer’s Association. The discovery builds on previous research from several NIA-funded laboratories that identified mutations in the Alzheimer’s disease related gene presenilin-1 as the cause of impaired activity and reduced health of nerve cell in the brain. The study’s lead investigator, Peter Koulen, Ph.D., of the IAADR at the University of North Texas Health Science Center had two major goals when he initiated the study in 2003: to identify the role of normal, so-called wild-type presenilin-1 in regulating neuronal function, and to reach the mechanism that drives this function. This appeared to be of particular relevance because only a small portion of Alzheimer’s disease sufferers carries such mutations (often called familial Alzheimer’s disease), while the majority of patients have sporadic Alzheimer’s disease, in which no apparent direct genetic changes have been identified.

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2 proteins in cardiovascular system pose a double whammy in Alzheimer’s

A new study has identified two proteins that cause patients with Alzheimer’s disease to face the double whammy of a lessened blood flow in the brain and reduced rate of brain’s ability to remove amyloid beta. The researchers behind the study have revealed that the two proteins work in tandem in the brain’s blood vessels.

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Brain ‘trick’ offers treatment hope for Alzheimer’s

Scientists in the UK and Canada have made a significant step forward in the search for new drugs to treat Alzheimer’s disease. An ageing population means that neurodegeneration, such as Alzheimer’s disease, is one of the major health problems in the developed world. But researchers at the University of York and Simon Fraser University in Burnaby, British Columbia, have designed an enzyme inhibitor which could ‘trick’ the brain and so help to halt neurodegeneration.

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Study identifies toxic key to Alzheimer’s disease memory loss

The team of Irish and international researchers have identified that the accumulation of a particular protein (called amyloid Ŗ-protein - AŖ) in the brain initiates Alzheimer’s disease and that it directly alters the structure and function of brain cells. The findings place a significant emphasis on the development of new therapeutic strategies targeted at the reduction of the formation of AŖ as opposed to the reduction of the plaque burden associated with the disease.

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Columbia researchers identify brain network that may help prevent or slow Alzheimer's

Columbia University Medical Center researchers, led by principal investigator Yaakov Stern, Ph.D., a professor at the Taub Institute for the Research on Alzheimer's Disease and the Aging Brain, have identified a brain network within the frontal lobe that is associated with cognitive reserve, the process that allows individuals to maintain function despite brain function decline due to aging or Alzheimer's disease.

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Splenic ellipsoids might be significant in the early development of AA amyloidosis

During the course of her PhD studies, Randi SÝrby demonstrated that ellipsoids, small filtering units for blood in the spleen, might be significant in the development of AA amyloidosis. AA amyloidosis is a potential complication of chronic inflammation or infection, for example, rheumatoid arthritis and tuberculosis, and is characterised by systematic deposition of protein fibrils in the tissues of organs such as the spleen and liver. Similar deposition, but of other proteins, also occurs in diseases such as Alzheimer's disease, Parkinson’s disease, and prion-associated disease ("mad cow disease"). In her thesis, Randi SÝrby used experimental amyloidosis in the mink as a model to study how amyloid deposition arises in different parts of the spleen. This model was chosen because the mink has especially well-developed ellipsoids, which are lacking in the more commonly-used experimental animals such as mouse and rat, but which are found in most other mammals, including man. Studies have shown that ellipsoids are central structures in amyloid deposition and that they play an early role in the development of the disease.

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The Scandal That is Alzheimer's Research

Back in 2004, I wrote three columns (when I was at The Wall Street Journal) on how one particular theory of what causes this awful disease—and therefore the best approach for treating it—has had the field in a headlock, censoring competing theories. That closed-mindedness, I quoted scientists as saying, had a lot to do with why there is not only no cure or preventive for Alzheimer’s, but not even a treatment that slows down the inexorable cognitive decline.

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Antipsychotics Bring Little Long-Term Benefit in Alzheimer's

At week 12, investigators found no significant differences between patients treated with an antipsychotic medication and those treated with placebo in scores on measures of cognition, function, and quality of life.

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A protein that protects against Alzheimer's?

Research on the mechanisms involved in neurodegenerative diseases such as Alzheimer's, stroke, dementia, Parkinson's and multiple sclerosis, to name a few, has taken a step forward thanks to the work of biological sciences Ph.D. student Sonia Do Carmo, supervised by Professor …ric Rassart of the Universitť du Quťbec ŗ Montreal (UQAM) Biological Sciences Department, in collaboration with researchers at the Armand-Frappier Institute and the University of Valladolid in Spain. Do Carmo and her collaborators have successfully demonstrated the protective and reparative role of apolipoprotein D, or ApoD, in neurodegenerative diseases. Their discovery suggests interesting avenues for preventing and slowing the progression of this type of illness. These studies were inspired by work done ten years ago by Professor Rassart's team, who then discovered increased levels of ApoD in the brains of people with several types of neurodegenerative disorders, including Alzheimer's. The team hypothesized that this protein might play a protective and restorative role but were unable to demonstrate this at the time.

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Destroying amyloid proteins with lasers

Researchers have found that a technique used to visualize amyloid fibers in the laboratory might have the potential to destroy them in the clinic. The technique involves zapping the fluorescently-tagged fibers with a laser, which can inhibit their growth and degrade them. This study, appearing in this week's JBC, may offer a non-drug alternative to treat amyloid-based disorders like Alzheimer, Parkinson, and Huntington diseases. Yuji Goto and colleagues had been studying amyloids, dense tangles of protein, to better understand how they form. In an effort to view amyloid formation under a microscope in real-time, they added an amyloid specific dye called thioflavin T (ThT) to the tangles and then hit it with a laser beam to induce fluorescence. Surprisingly, they found that under the right conditions, the laser could actually stop fiber growth and even degrade the amyloids.

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Collagen VI may help protect the brain against Alzheimer's disease

Scientists from the Gladstone Institute of Neurological Disease (GIND), UCSF, and Stanford have discovered that a certain type of collagen, collagen VI, protects brain cells against amyloid-beta (A?) proteins, which are widely thought to cause Alzheimer's disease (AD). While the functions of collagens in cartilage and muscle are well established, before this study it was unknown that collagen VI is made by neurons in the brain and that it can fulfill important neuroprotective functions. The team of investigators led by GIND director Lennart Mucke, MD, reported in the current edition of the journal Nature Neuroscience, that collagen VI is increased in brain tissues of Alzheimer's patients."We first noticed the increase in collagen VI in the brain of AD mouse models, which inspired us to look for it in the human condition and to define its role in the disease," said Dr. Mucke. The Gladstone team had profiled changes in gene expression using DNA microarrays, which provides an unbiased method for identifying key biological pathways. By comparing all of the genes that are active in disease and normal tissue, one can get valuable information on new pathways and potential therapeutic targets. The researchers looked at the dentate gyrus, a specific area of the brain that is critical to memory and particularly vulnerable in AD, and compared the genes that were turned on and off in normal mice and a mouse model of AD. This analysis revealed the striking increase in collagen VI in the brains of mice that model AD.

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Antipsychotic drugs double risk of death among Alzheimer’s patients

New research into the effects of antipsychotic drugs commonly prescribed to Alzheimer’s patients concludes that the medication nearly doubles risk of death over three years. The study, funded by the Alzheimer’s Research Trust, was led by Prof Clive Ballard’s King’s College London team and is published in Lancet Neurology on 9 January. The study involved 165 Alzheimer’s patients in care homes who were being prescribed antipsychotics. 83 continued treatment and the remaining 82 had it withdrawn and were instead given oral placebos.

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New Alzheimer's findings

High stress levels may contribute to memory loss among people at risk for developing Alzheimer's disease. The Ś4 variant of the apolipoprotein E (APOE) gene contributes to the risk for memory loss related to Alzheimer's disease.

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Ionophore reverses Alzheimer's within days in mouse models

Scientists report a remarkable improvement in Alzheimer's transgenic mice following treatment with a new drug. The study, published by Cell Press in the July 10th issue of the journal Neuron, provides the first demonstration that an ionophore, a compound that transports metal ions across cell membranes, can elicit rapid and pronounced improvement in neuropathology and cognitive function in mouse models of Alzheimer's Disease (AD). Recent research has implicated dysregulation of metal ions in the brain, particularly copper and zinc, in the pathogenesis of AD and the damaging accumulation of amyloid beta (A?) protein that is characteristic of this devastating disease. The ionophore clioquinol (CQ), an 8-hydroxyquinoline, has been shown to increase intracellular copper and zinc levels and decrease A? levels in cultured cells and in the brains of transgenic (Tg) AD mice. However, further studies in mice and humans demonstrated that brain entry of CQ was quite limited.

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Study points to cocktail therapy for Alzheimer's

A dietary cocktail that includes a type of omega-3 fatty acid can improve memory and learning in gerbils, according to the latest study from MIT researchers that points to a possible beverage-based treatment for Alzheimer's and other brain diseases.

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Mayo Clinic Researchers Find that Variants in a Gene on the X Chromosome are Associated with Increased Susceptibility to Alzheimer's Disease

Researchers at Mayo Clinic have discovered the first gender-linked susceptibility gene for late-onset Alzheimer's disease.In the Jan. 11 online edition of Nature Genetics, they report the results of their two-stage genome-wide association study of patients with Alzheimer's disease. The research showed that women who inherited two copies of a variant in the PCDH11X gene, found on the X chromosome, are at considerably greater risk of developing Alzheimer's disease. Women with a variant on one of their two X chromosomes also had some increase in risk, as did men with the variant on their single X chromosome, but these effects were weaker than inheriting two variants.

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Calcium may be the key to understanding Alzheimer's disease

Researchers at the University of Pennsylvania School of Medicine have shown that mutations in two proteins associated with familial Alzheimer's disease disrupt the flow of calcium ions within neurons. The two proteins, called PS1 and PS2 (presenilin 1 and 2), interact with a calcium release channel in an intracellular cell compartment.

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Possible Alzheimer's Disease Marker Discovered in Rare Genotype

Researchers at Banner Health's Sun Health Research Institute have uncovered evidence that Alzheimer's disease (AD) may be clinically confirmed in patients with apolipoprotein E2 homozygote. The results of their study are published in the January 2009 issue of the Journal of Alzheimer's Disease.

Apolipoprotein E2 homozygote has been associated with a protective effect against AD and contributes to delaying the onset of symptoms. However previously, no significant data had pointed to clinically confirmed AD in persons with apolipoprotein E2 homozygote. The reverse is true of apolipoprotein E4. Previous studies have confirmed that apolipoprotein E4 is a predictive risk factor for AD and indicates an increased genetic risk of AD.

Clinical confirmation of the apolipoprotein E2 homozygote Alzheimer's disease finding in this study was confirmed by MRI, PET and neuropsychological evaluation and testing. AD pathology is yet to be determined and will occur at post mortem.

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Early study reveals promising Alzheimer's disease treatment

A drug once approved as an antihistamine in Russia improved thinking processes and the ability to function in patients with Alzheimer's disease in a study conducted there, said an expert at Baylor College of Medicine in Houston. The findings are published in the current issue of the journal The Lancet.

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New step in DNA damage response in neurons discovered

Researchers have identified a biochemical switch required for nerve cells to respond to DNA damage. The finding, scheduled for advance online publication in Nature Cell Biology, illuminates a connection between proteins involved in neurodegenerative disease and in cells' response to DNA damage. Most children with the inherited disease ataxia telangiectasia are wheelchair-bound by age 10 because of neurological problems. Patients also have weakened immune systems and more frequent leukemias, and are more sensitive to radiation. The underlying problem comes from mutations in the ATM (ataxia telangiectasia mutated) gene, which encodes an enzyme that controls cells' response to and repair of DNA damage. ATM can be turned on experimentally by treating cells with chemicals that damage DNA. After other proteins in the cell detected broken DNA needing repair, scientists had thought that the ATM protein could activate itself directly. Emory researchers have shown that an additional step is necessary first. "In neurons that are not dividing anymore, we now know that another regulator is involved: Cdk5," says Zixu Mao, MD, PhD, associate professor of pharmacology and neurology at Emory University School of Medicine. Working with postdoctoral fellows Bo Tian, PhD and Qian Yang, PhD, Mao found that the Cdk5 protein must activate ATM before ATM can do its job in neurons. The results support the idea that Cdk5 may be a potential drug target. Cdk5 contributes to normal brain development, and aberrant Cdk5 activity is known to be involved in the death of neurons in several neurodegenerative diseases, including Alzheimer's, Parkinson's and amyotrophic lateral sclerosis.

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Scientists demonstrate means of reducing Alzheimer's-like plaques in fly brain

Neuroscientists at Cold Spring Harbor Laboratory are part of a collaboration that has succeeded in demonstrating that overexpression of an enzyme in the brain can reduce telltale deposits causally linked with Alzheimer's disease.

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Video released of rapid Alzheimer's improvement after new immune-based treatment

New research into the treatment of Alzheimer's disease reports improvement in language abilities using a novel immune-based approach. A video accompanying the research, published today in the open access journal BMC Neurology, documents rapid language improvement within minutes of using this new treatment.

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Isotonic seawater and Alzheimer

The Ocean Water properties as supplemental food are giving excellent results in the sports field and in other areas of human activity, for which we hope that it will be very positive for Alzheimer patients.

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An ID for Alzheimer's?

In furthering the steps toward that goal, UCLA associate professor of neurology John Ringman and his colleagues confirm in the current issue of the journal Neurology that during Alzheimer's earliest stages, levels of specific proteins in the blood and spinal fluid begin to drop as the disease progresses, making them potentially useful as biomarkers to identify and track progression long before symptoms appear.

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New study provides further evidence that apple juice can delay onset of Alzheimer's disease

A growing body of evidence demonstrates that we can take steps to delay age-related cognitive decline, including in some cases that which accompanies Alzheimer's disease, according to a study published in the January 2009 issue of the Journal of Alzheimer's Disease. Thomas B. Shea, PhD, of the Center for Cellular Neurobiology; Neurodegeneration Research University of Massachusetts, Lowell and his research team have carried out a number of laboratory studies demonstrating that drinking apple juice helped mice perform better than normal in maze trials, and prevented the decline in performance that was otherwise observed as these mice aged. In the most recent study Shea and his team demonstrated that mice receiving the human equivalent of 2 glasses of apple juice per day for 1 month produced less of a small protein fragment, called "beta-amyloid" that is responsible for forming the "senile plaques" that are commonly found in brains of individuals suffering from Alzheimer's disease.

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Alzheimer's helmet therapy hope

An experimental helmet is being tested by scientists as a treatment for Alzheimer's disease. It delivers low levels of infra-red light, which researchers at the University of Sunderland, believe may stimulate the growth of brain cells.

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New study finds healthy children of Alzheimer patients show early brain changes

Medical College of Wisconsin researchers in Milwaukee have reported that children of Alzheimer's patients who are carriers of a genetic risk factor for Alzheimer's disease have neurological changes that are detectable long before clinical symptoms may appear.

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UIC chemists characterize Alzheimer's neurotoxin structure

A team of UIC chemists has characterized the molecular structure of the intermediate stage of plaque-forming amyloid fibrils, believed to cause Alzheimer's disease. The finding may lead to new drug targets for this and other amyloid diseases, such as Parkinson's and Creutzfeldt-Jakob.

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Thyroid Hormone May Boost Women's Alzheimer's Risk

High or low levels of the hormone thyrotropin may be associated with an increased risk of Alzheimer's disease in women. Thyrotropin affects thyroid gland function and thyroid hormone levels.

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Researchers Find Use of Angiotensin Receptor Blockers are Associated with Lower Incidence, Progression of Alzheimer’s Disease

Researchers at Boston University School of Medicine (BUSM) have, for the first time, found that angiotensin receptor blockers (ARBs)—a particular class of anti-hypertensive medicines—are associated with a striking decrease in the occurrence and progression of dementia. Data from this study will be presented this weekend (July 27) at the 2008 International Conference on Alzheimer’s disease in Chicago.

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Consumption of fruits may reduce the risk of Alzheimer's disease

Apples, bananas, and oranges are the most common fruits in both Western and Asian diets, and are important sources of vitamins, minerals, and fiber. A new study in the Journal of Food Science explores the additional health benefits of these fruits and reveals they also protect against neurodegenerative diseases, including Alzheimer's disease.

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Alzheimer's disease patients show improvement in trial of new drug

A new drug has been shown to improve the brain function of people with early stage Alzheimer's disease and reduce a key protein associated with the disease in the spinal fluid, in a small study published today in the journal Lancet Neurology and presented at the 2008 Alzheimer's Association International Conference on Alzheimer's Disease.

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Sugary beverages increase risk of Alzheimer's disease

Drinking sugary beverages like soda may increase risk of Alzheimer's disease, according to a new study published in the Dec. 14, 2007 issue of Journal of Biological Chemistry.

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Signs of Alzheimer's disease may be present decades before diagnosis

Scientists from the University of South Florida and the University of Kentucky report that people who develop Alzheimer's disease may show signs of this illness many decades earlier in life, including compromised educational achievement.

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PET scans may help assess presence of brain plaques related to Alzheimer's disease

A type of positron emission tomography (PET) scanning may be useful in a non-invasive assessment of the formation of Alzheimer’s disease–related plaques in the brain, according to small study posted online today that will appear in the October 2008 print issue of Archives of Neurology, one of the JAMA/Archives journals. Plaques in the brain made of beta-amyloid and other compounds are considered hallmarks of the development of Alzheimer’s disease, according to background information in the article. Currently, the only reliable way to assess the aggregation of these compounds in the brain is through analyzing brain tissue samples obtained during life or autopsy after death—“a major methodological obstacle considering clinical drug trials of early Alzheimer’s disease,” the authors note.

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Bacterial Inclusion Bodies Contain Amyloid-Like Structure

Protein aggregation is a process in which identical proteins self-associate into imperfectly ordered macroscopic entities. Such aggregates are generally classified as amorphous, lacking any long-range order, or highly ordered fibrils. Protein fibrils can be composed of native globular molecules, such as the hemoglobin molecules in sickle-cell fibrils, or can be reorganized ?-sheet–rich aggregates, termed amyloid-like fibrils. Amyloid fibrils are associated with several pathological conditions in humans, including Alzheimer disease and diabetes type II. We studied the structure of bacterial inclusion bodies, which have been believed to belong to the amorphous class of aggregates. We demonstrate that all three in vivo-derived inclusion bodies studied are amyloid-like and comprised of amino-acid sequence-specific cross-? structure. These findings suggest that inclusion bodies are structured, that amyloid formation is an omnipresent process both in eukaryotes and prokaryotes, and that amino acid sequences evolve to avoid the amyloid conformation.

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Iron banded worms drying out of blood could be linked to Parkinson's and Alzheimer's

Researchers at the University of Warwick and the Indian Institute of Technology Kanpur have discovered that the mechanism that we rely on to transport iron safely through our blood can collapse into a state which grows long worm-like "fibrils" banded by lines of iron rust. This process could provide the first insight into how iron gets deposited in the brain to cause some forms of Parkinson's & Alzheimer's and Huntington's diseases.

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Physical frailty may be linked to Alzheimer's disease

Physical frailty, which is common in older persons, may be related to Alzheimer's disease pathology, according to a study published in the Aug. 12, 2008, issue of Neurology, the medical journal of the American Academy of Neurology.

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Moss protein plays role in Alzheimer's disease

Preventing Alzheimer's from developing is a goal of Raphael Kopan, Ph.D., professor of molecular biology and pharmacology at the Washington University in St. Louis School of Medicine. The moss plant studied in the laboratory of Ralph S. Quatrano, Ph.D., Spencer T. Olin Professor of biology, might inch Kopan toward that goal. Through collaboration, the researchers have found that a gene in moss is also structurally conserved in AD and has similar functions.

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Why fish oil is good for you

UCLA researchers report that omega-3 fatty acid docosahexaenoic acid, found in fish oil, increases the production of LR11, a protein that is found at reduced levels in Alzheimer's patients and which is known to destroy the the "plaques" associated with the disease.

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Tampa Researchers Find Caffeine Eases Alzheimer's Effects

Given the already widespread use and acceptance of coffee in moderate amounts," they wrote, "long-term coffee intake could be a viable strategy" for reducing the risk of Alzheimer's disease.

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Diets of Alzheimer's patients lack many nutrients

People with Alzheimer's disease eat less nutritiously than their peers without dementia, even in the early stages of the disease, new research from Canada shows.

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Red, red wine - How it fights Alzheimer's

Scientists call it the "French paradox" — a society that, despite consuming food high in cholesterol and saturated fats, has long had low death rates from heart disease. Research has suggested it is the red wine consumed with all that fatty food that may be beneficial — and not only for cardiovascular health but in warding off certain tumors and even Alzheimer's disease. Now, Alzheimer's researchers at UCLA, in collaboration with Mt. Sinai School of Medicine in New York, have discovered how red wine may reduce the incidence of the disease. Reporting in the Nov. 21 issue of the Journal of Biological Chemistry, David Teplow, a UCLA professor of neurology, and colleagues show how naturally occurring compounds in red wine called polyphenols block the formation of proteins that build the toxic plaques thought to destroy brain cells, and further, how they reduce the toxicity of existing plaques, thus reducing cognitive deterioration. Polyphenols comprise a chemical class with more than 8,000 members, many of which are found in high concentrations in wine, tea, nuts, berries, cocoa and various plants. Past research has suggested that such polyphenols may inhibit or prevent the buildup of toxic fibers composed primarily of two proteins — AŖ40 and AŖ42 — that deposit in the brain and form the plaques which have long been associated with Alzheimer's. Until now, however, no one understood the mechanics of how polyphenols worked.

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Fast food a potential risk factor for Alzheimer’s

Mice that were fed a diet rich in fat, sugar and cholesterol for nine months developed a preliminary stage of the morbid irregularities that form in the brains of Alzheimer’s patients. The study results, published in a doctoral thesis from the Swedish medical university Karolinska Institutet (KI), give some indications of how this difficult to treat disease might one day be preventable.Alzheimer’s is the most common form of dementia, there being roughly 90,000 patients with the disease in Sweden today. The underlying causes of Alzheimer’s disease are still something of a mystery, but there are a number of known risk factors. The most common is a variant of a certain gene that governs the production of apolipoprotein E, one of the functions of which is to transport cholesterol. The gene variant is called apoE4 and is found in 15-20 per cent of the population.For her doctoral thesis, Susanne Akterin studied mice that had been genetically modified to mimic the effects of apoE4 in humans. The mice were then fed for nine months on a diet rich in fat, sugar and cholesterol, representing the nutritional content of most fast food.“On examining the brains of these mice, we found a chemical change not unlike that found in the Alzheimer brain,” says Ms Akterin, postgraduate at KI Alzheimer’s Disease Research Center.

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Memantine and Alzheimer's disease

In a study published in the Journal of Alzheimer's Disease, researchers from the University of Aberdeen report that the drug memantine, used for the treatment of Alzheimer's disease and praised as "the first and only representative of a new class of Alzheimer drugs" works in fact similar to other existing compounds, and is beneficial only in a narrow concentration range. They further indicate that the complex pharmacological profile of memantine requires careful consideration concerning suitable doses and suitable patient groups.

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Mutant proteins result in infectious prion disease in mice

A worldwide group of scientists, including Christina J. Sigurdson, D.V.M., Ph.D., assistant professor of pathology at the UCSD School of Medicine, has created an infectious prion disease in a mouse model, in a step that may help unravel the mystery of this progressive disease that affects the nervous system in humans and animals. The study, led by Professor Dr. Adriano Aguzzi of the Institute of Neuropathology at the University of Zurich in Switzerland, was designed to investigate the specific changes in the prion protein that may contribute to chronic wasting disease (CWD). CWD is a highly infectious prion disease found in free-ranging deer and elk that is similar to bovine spongiform encephalopathy (BSE, or "mad cow disease") in cattle and Creutzfeldt-Jakob disease in humans. Prion diseases are thought to be a result of a misfolded form of the prion protein that induces formation of amyloid plaques in the brain – changes that are also seen in patients with Alzheimer's disease.

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Treating Sleep Apnea in Alzheimer’s Patients Helps Cognition

Continuous positive airway pressure (CPAP) treatment seems to improve cognitive functioning in patients with Alzheimer’s disease who also suffer from obstructive sleep apnea, according to the results of a randomized clinical trial conducted at the University of California, San Diego. The study – led by Sonia Ancoli-Israel, Ph.D., professor of psychiatry at the UC San Diego School of Medicine and one of the nation’s preeminent experts in the field of sleep disorders and sleep research in aging populations – was published in the November issue of the Journal of the American Geriatrics Society.

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New study identifies link between Alzheimer's disease biomarkers in healthy adults

A study published in the November issue of the Journal of Alzheimer's Disease provides an insight into normal, physiological levels and association between proteins involved in development of Alzheimer's disease. A group of scientists and physicians from the University of Washington and Puget Sound Veterans' Affairs Health Care System in Seattle, in collaboration with groups from the University of Pennsylvania and the University of California San Diego, performed a study in cognitively normal and generally healthy adults, from young to old (age range 21-88 years), of both genders, measuring levels of different brain-derived molecules associated with Alzheimer's disease. Investigators determined that cerebrospinal fluid (CSF) levels of apolipoprotein E (apoE), one of the most important proteins involved in transfer of fatty substances between different brain cells, are highly correlated with the levels of proteins known to be involved in development of Alzheimer's disease, amyloid precursor protein (APP) and tau. While many studies have previously shown that apoE gene is very important for Alzheimer's disease development, the connection between apoE protein and other relevant CSF markers in healthy adults was not known. Although this type of study cannot establish causal associations, the results strongly suggest that the CSF levels of apoE may explain a significant proportion of the levels of APP- and tau-related biological markers in the healthy human brain, indicating a strong physiological link between apoE, APP and tau. In other words, the study points to a possibility that modulation of the levels of apoE may affect the levels of APP and tau in the brain.

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New method developed to identify genetic determinants of Alzheimer's disease

A rapid and accurate DHPLC assay for determination of apolipoprotein E genotypes has been developed by researchers from the Department of Medical Genetics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. This assay combines PCR and DHPLC and can be used to conduct efficient genotyping of the human population, which in turn will help in the diagnosis and treatment of Alzheimer’s disease. A description of the assay has been published this month in the Journal of Alzheimer's Disease.

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Lead Link To Alzheimer's Disease?

Lead poisoning in infancy may make Alzheimer's disease more likely decades later, a new study shows.

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