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Ziekte van Alzheimer


Narcose stof Isofluraan veroorzaakt Alzheimer veranderingen in de hersenen

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.

Lees artikel

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Isofluraan is een damp (narcosegas) die men kan gebruiken voor algemene anesthesie. Momenteel neemt het gebruik in Nederland af door de opvolging van nieuwere dampen zoals desfluraan en sevofluraan. Het is samen met enfluraan de opvolgende generatie van halothaan.


Snelle verbetering van Alzheimer met nieuwe immuunbehandeling

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.

http://www.biomedcentral.com/content/pdf/1471-2377-8-27.pdf

http://www.tobinick.com/


Vetten in de hersenen van belang bij de ziekte van Alzheimer? Vlaamse wetenschappers kraken de code

Brussel, Leuven – De ziekte van Alzheimer is de meest voorkomende vorm van dementie in de
Westerse wereld, met enorme implicaties voor een vergrijzende samenleving. Algemeen wordt
aangenomen dat de aandoening wordt veroorzaakt door zogehete protofibrillen van het
Alzheimerpeptide (A -peptide). Het was tot nu toe niet bekend onder welke omstandigheden
deze protofibrilvorm ontstaat en de ziekte veroorzaakt. VIB-onderzoekers hebben nu ontdekt
dat specifieke vetten, die ook voorkomen in onze hersenen, de vorming van deze protofibrillen
in de hand werken. Deze ontdekking is erg belangrijk omdat het een nieuwe piste opent in de
zoektocht naar geneesmiddelen tegen de ziekte van Alzheimer. Bovendien veklaart dit
onderzoek eerdere aanwijzingen over een verband tussen vetten en de ziekte van Alzheimer.

Verkeerde opvouwing van eiwitten: oorzaak van verschillende ziekten
De biologische functie van cellen hangt af van de juiste opvouwing van duizenden eiwitten. De cel corrigeert normaal gezien automatisch een verkeerde opvouwing van eiwitten. Bij ziekten zoals de ziekte van Alzheimer, de ziekte van Parkinson en de ziekte van Creutzfeld Jacob, leidt een slechte opvouwing echter tot het neerslaan van die eiwitten in weefsels. Bij de ziekte van Alzheimer – de meest voorkomende vorm van dementie die in België alleen al zo’n 100 000 mensen treft - leidt de slechte opvouwing van het A - amyloide peptide in verschillende stappen tot de vorming van plakken. Deze plakken zijn een opeenstapeling van zogenaamde fibrillen en zijn op zich niet toxisch. Een van de tussenstappen bij de aanmaak van plakken is de vorming van de protofibrilvorm van het A -peptide. Protofibrillen zijn wel toxisch voor de hersencellen. De vergiftigde cellen sterven af en dit veroorzaakt geheugenverlies. Daarom worden deze protofibrillen beschouwd als de belangrijkste verantwoordelijke voor de symptomen van de ziekte van Alzheimer.

Alom aanwezige hersenvetten destabiliseren plakken
VIB-onderzoekers slaagden erin om met behulp van specifieke vetten de fibrillen om te zetten tot
protofibrillen. Dit tot ieders verbazing. Algemeen wordt immers al jaren aangenomen dat de fibrillen – en de plakken die ze veroorzaken – stabiel zijn en dus, eens ze gevormd zijn, niet meer verdwijnen of omgevormd worden tot een andere structuur. Ivo Martins, Joost Schymkowitz en Frederic Rousseau (VIB, Vrije Universiteit Brussel), en Inna Kupperstein en Bart De Strooper (VIB, K.U.Leuven) tonen nu aan dat de aanwezigheid van specifieke vetten die normaal in de hersenen voorkomen, kan leiden tot destabilisatie van de fibrillen, en dus van de plakken die zo typerend zijn voor de ziekte van Alzheimer. De vrijgekomen protofibrillen zijn toxisch voor de hersencellen, waardoor deze cellen – althans in vitro - afsterven. Dat dit ook in werkelijkheid het geval is, konden de wetenschappers aantonen door de protofibrillen bij proefdieren (muizen) in te spuiten. Dit veroorzaakte geheugenverlies bij deze muizen. De onderzoekers verklaren dat deze symptomen vergelijkbaar zijn met die van beginnende dementie bij de mens.

Protofibrillen produceren voor nieuwe geneeskundige toepassingen
Deze ontdekking opent een nieuw spoor in de zoektocht naar mogelijke geneesmiddelen tegen de ziekte van Alzheimer. Het wijst immers aan dat stoffen die de toxiciteit of vorming van de protofibrillen neutraliseren, gebruikt zouden kunnen worden als geneesmiddel tegen de ziekte van Alzheimer. Met de ontdekking van een methode om toxische protofibrillen aan te maken, leveren de VIB-onderzoekers een goed model om geneesmiddelen te ontdekken die de vorming van protofibrillen kunnen tegengaan.

Daarnaast hebben ze met dit onderzoek aangetoond dat de vetconcentratie in de hersenen blijkbaar een belangrijke impact heeft op een biologisch evenwicht tussen de niet-toxische plakken en de toxische oligomeren. Deze resultaten leiden tot nieuwe onderzoekspistes om het belang van de vethuishouding voor ziekten zoals de ziekte van Alzheimer te onderzoeken.

Dit onderzoek toont duidelijk de meerwaarde aan van de bundeling van de expertise van verschillende onderzoeksgroepen. Deze belangrijke resultaten zijn immers het gevolg van een nauwe samenwerking tussen onderzoekers van het VIB SWITCH-laboratorium, Vrije Universiteit Brussel, en het VIB-departement Ontwikkelings- en Moleculaire Genetica, K.U.Leuven.

Relevante wetenschappelijke publicatie
Het onderzoek staat op de website van het toonaangevende tijdschrift The EMBO Journal
(www.nature.com/emboj/journal/vaop/ncurrent/index.html): Martins et al., Lipids revert inert A amyloid fibrils to neurotoxic protofibrils that affect learning in mice


TV - Zomergasten - Christine van Broeckhoven over Alzheimer

De Vlaamse hoogleraar dr. Christine van Broeckhoven (1953) is een internationale autoriteit in genetisch onderzoek naar Alzheimer-dementie en andere hersenaandoeningen. Alzheimer-dementie is volgens Van Broeckhoven het ergste wat een mens kan overkomen; één op de vier bejaarden krijgt met de ziekte te maken. Na haar studie scheikunde en biochemie en haar doctoraat in de moleculaire biologie richtte zij in 1989 aan de Universiteit van Antwerpen haar eigen laboratorium voor moleculaire genetica op, waar inmiddels 80 mensen werken, en waarvan zij wetenschappelijk directeur is. Van Broeckhoven heeft in alle vooraanstaande tijdschriften op haar vakgebied gepubliceerd en kreeg voor haar werk talloze wetenschappelijke prijzen en onderscheidingen, zoals de Vijfjaarlijkse Prijs voor Wetenschappelijk Onderzoek van het Vlaamse Fonds Wetenschappelijk Onderzoek en - als eerste Europese vrouw - de prestigieuze Potamkin Prize van de American Academy of Neurology.

Ook ontving ze in 2006 de l'Oréal/Unesco Honor Award for Women in Science en werd ze benoemd tot grootofficier in de Leopoldsorde, een van de hoogste Belgische koninklijke onderscheidingen. Bij de federale verkiezingen in België op 10 juni van dit jaar was Van Broeckhoven lijsttrekker voor de SP.a (Socialistische Partij Anders) in Antwerpen. Speerpunten in haar campagne waren de vergrijzing van de bevolking en de positie van vrouwen. Ze werd met ruim 26.000 stemmen gekozen in de Kamer van Volksvertegenwoordigers. Op 28 juni wordt ze geïnaugureerd als Kamerlid. Presentatie: Joris Luyendijk.

http://player.omroep.nl/?aflID=5276058&


Bloedtest voor Alzheimer

Bepaalde eiwitten in het bloed kunnen een indicatie zijn van een verhoogd risico op de ziekte van Alzheimer volgens nieuw onderzoek in het journaal Brain. Het is de eerste keer dat onderzoekers markers in het bloed hebben gevonden om zo de ontwikkeling van Alzheimer op te sporen.

http://www.kcl.ac.uk/phpnews/wmview.php?ArtID=1459


Marihuana en Alzheimer

Doe je er als Amerikaanse overheid alles aan om marihuana gebruik hard aan te pakken en gebruikers als criminelen af te schilderen (wapenbezit is echter geen probleem !) en dan komt er een studie naar buiten dat er een stofje in zit dat beter werkt dan de bestaande medicatie voor Alzheimer. Wordt het straks nog blowen op je oude dag.....

A Molecular Link between the Active Component of Marijuana and Alzheimer's Disease Pathology

Departments of Chemistry, Immunology, and Molecular Biology, Molecular and Integrated Neurosciences Department, The Skaggs Institute for Chemical Biology, and Worm Institute for Research and Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037

Alzheimer's disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer's disease are expected to triple over the next 50 years. Consequently, the development of treatments that slow or halt the disease progression have become imperative to both improve the quality of life for patients and reduce the health care costs attributable to Alzheimer's disease. Here, we demonstrate that the active component of marijuana, 9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid -peptide (A) aggregation, the key pathological marker of Alzheimer's disease. Computational modeling of the THC-AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis. Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of A aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.

http://pubs.acs.org/cgi-bin/abstract.cgi/mpohbp/asap/abs/mp060066m.html


Medicijnen tegen de symptomen van de ziekte van Alzheimer werken
bij meeste patiënten niet

In Amerika is er een grootschalige studie gedaan naar medicijnen die veel gebruikt worden bij Alzheimer patiënten die snel geirriteerd of agressief zijn. De medicijnen die nu veel gebruikt worden werken slechts bij een kleine groep mensen en zijn niet effectief genoeg om bij een grote groep gebruikt te worden aldus de onderzoekers. Dit soort medicijnen wordt normaal gebruikt bij behandeling van schizofrenie en bipolaire stoornissen (stemmingsstoornissen). Deze medicijnen worden ook vaak ingezet bij de ziekte van Alzheimer omdat er geen goedgekeurde medicijnen zijn voor deze symptomen bij demente patiënten, dokter grijpen dan vaak naar deze medicijnen. In het onderzoek werd er gewerkt met een placebo en olanzapine (Zyprexa), quetiapine (Seroquel), en risperidone (Risperdal).

http://www.urmc.rochester.edu/pr/news/story.cfm?id=1255


Stof uit alg kan mogelijk helpen bij Alzheimer

Zwitserse onderzoekers van het Federal Institute of Technology in Zurich hebben een stof geisoleerd uit blauwgroene algen die mogelijk de basis van een nieuw medicijn kan worden tegen de ziekte van Alzheimer en andere hersenaandoeningen.

Dit is de eerste keer dat onderzoekers een waardevolle stof uit dit type cyanobacterie hebben kunnen onttrokken, het onderzoek hiernaar zal nog veel geld en tijd gaan kosten. De gevonden stof heet nostocarboline en wordt gehaald uit de Nostoc blauwgroene alg.

http://www.swissinfo.org/eng/science_technology/detail/


Multivitamines met koper - gevaarlijk in combinatie met slechte vetten

Regelmatig kom ik artikelen tegen waarin men waarschuwt voor multivitamines die veel ijzer of vitamine A bevatten. Teveel ijzer in het lichaam kan een rol spelen bij oa het krijgen van kanker en teveel vitamine A kan tot botbreuken leiden, je lever beschadigen, je cholesterol verhogen en is gevaarlijk voor het ongeboren kind. Een bekend acne medicijn op Vitamine A basis is Accutane. Dit omstreden middel krijgt de laatste tijd veel negatieve publiciteit.

Maar nu komen de multivitamines opnieuwnegatief in beeld. Het blijkt namelijk dat ouderen (65+) die zowel slechte vetten eten (verzadigd vet en transvetten) en tegelijkertijd veel koper binnenkrijgen mentaal 1.5 keer sneller verouderen dan leeftijdgenoten. Dit betekent dus ook een verhoogde kans op ziekten zoals Alzheimer. De mensen die hoge koper levels in hun bloed hadden bleken meestal mensen te zijn die extra koper binnen kregen via de bekende multivitamines. De normale dag dosis in Amerika is 0.9 mg terwijl de mensen die problemen kregen gemiddeld 2.75 mg per dag binnenkregen.

In Nederland heb ik sinds enkele maanden kontakt met een gepensioneerd neuroloog van het UMC, Drs Tjaard Hoogenraad, die ook beweert dat juist koper een belangrijke rol speelt bij de ziekte van Alzheimer. Hij wil dit dan ook graag verder onderzoeken maar loopt vast door gebrek aan geld voor een mogelijke klinische studie hiernaar. Ik wilde deze neuroloog helpen en heb de informatie online gezet op: www.alzheimer-copper.com

Als je dan ook weet dat zink en koper een balans zijn en dat veel mensen een zinktekort hebben dan gaat de koper dus nog meer overheersen. Volgens een artikel in Ortho magazine van Drs Gert Schuitemaker zorgt gewoon volkorenbrood ook voor een zinktekort. Het probleem is dat het fytinezuur in de granen de opname van met name zink/ijzer blokkeert. Alternatieven zijn dan zuurdesembrood en tarwekiembrood waarbij dit zuur grotendeels is afgebroken.

Samenvatting van de studie
http://archneur.ama-assn.org/cgi/content/short/63/8/1085

New York Times
http://www.nytimes.com/2006/08/22/health/nutrition/22agin.html

Science and Technology
http://www.sciam.com/article.cfm?chanID=sa003&articleID=

USA today
http://www.usatoday.com/tech/news/techinnovations/
2003-12-26-alz-advance_x.htm

Zinktekort door volkoren gistbrood
http://voeding.web-log.nl/voeding/2006/07/eten_van_volkor.html

Gevaren van teveel vitamine A door Accutane anti acne middel
http://www.mercola.com/2006/sep/9/accutane_harms_your_liver


Alzheimer en koper

Volgens de Nederlandse neuroloog Dr Tjaard Hoogenraad speelt vrij koper  (kopervergiftiging) een zeer belangrijke rol bij de ziekte van Alzheimer:

Bloedkoperziekte (hypercupremie) is een nieuwe naam voor kopervergiftiging die veroorzaakt wordt door een verhoogde concentratie van vrij koper in het bloed. Onder vrij koper verstaat men de fractie koper in het bloed die niet gebonden is aan het koperbindende eiwit ceruloplasmine. Vrij bloedkoper is schadelijk, terwijl het aan ceruloplasmine gebonden bloedkoper niet schadelijk is. Vrij koper in bloed kan de bloed-hersen-barriere passeren en is daardoor potentieel schadelijk voor hersencellen. In de hersenen komen eiwitten voor, zoals metallothioneine en ceruloplasmine die vrij koper onschadelijk maken waarbij het metaalion aan het eiwit te binden. Er zijn tot op heden twee neurodegeneratieve ziekten bekend waarbij verhoogde waarden van vrij koper in het bloed zijn beschreven: de ziekte van Wilson en de ziekte van Alzheimer. Bij beide aandoeningen wordt verondersteld dat het verhoogde gehalte van vrij koper in het bloed van oorzakelijke betekenis is voor de neurodegeneratieve afwijkingen.

http://www.alzheimer-copper.com


Het effect van koper op dieren

Koper speelt een rol in de ontwikkeling van de ziekte van Alzheimer door inductie van zuurstofradicalen als gevolg van binding van koper aan het amyloid ß-4 eiwit. Koper speelt een directe dan wel indirecte rol bij de verstoring van de oxidant – antioxidant balans, hetgeenresulteert in oxidatieve stress. (Proefschrift Ingeborg de Wolf)

http://mamb.ru/lib/topol/the%20various%20faces%
20of%20copper%20in%20laboratory%20animals.pdf


Aluminium de echte oorzaak van Alzheimer?

De Amerikaan Harold D. Foster beweert dat de echte oorzaak van Alzheimer wordt veroorzaakt door aluminium, met name bij een groep mensen die meer gevoelig zijn voor dit toxische metaal. Hij schreef hier een gratis boek over met een onderbouwing en informaties mbt vele studies die je kunt downloaden op zijn site. Ik ben helaas niet in staat om alle informatie die ik vind te vertalen maar alle hulp is welkom......

There is currently a global Alzheimer’s pandemic involving tens of millions of victims. In the USA alone, the number of those affected is expected to reach 14 million by 2050.1 This suffering and the financial costs associated with it are unnecessary. Alzheimer’s disease is caused by aluminum and is particularly common in those carrying the APO E4 allele(s), who are more susceptible to this toxic metal because they are less capable
than the general population of removing brain beta-amyloid and tau proteins. As a consequence, such individuals are at higher risk of developing Alzheimer’s disease, as these abnormal proteins build up in the brain and form neuritic plaques and neurofibrillary tangles.

Naturally, this process occurs more often and most rapidly in regions that promote the deposition of beta-amyloid and tau. Such “harmful” environments are those in which drinking water is acidic, high in monomeric aluminum, and lack magnesium, calcium, and silicic acid. Under these circumstances, aluminum enters the brain and impairs
various enzymes, including choline acetyltransferase, calcium/calmodulin kinase II, alkaline phosphatase, and phospholipase A2. The result of this process is the abnormal brain pathology seen in Alzheimer’s disease patients and the disrupted biochemistry
associated with it. In an earlier publication,2 I called this explanation of the downward spiral, known as Alzheimer’s disease, Foster’s Multiple Antagonist Hypothesis.

http://www.hdfoster.com/Foster_Alzheimers.pdf


Eiwit (aequorin) van kwal (jellyfish) kan mogelijk helpen bij Alzheimer/Parkinson

Volgens onderzoekers uit Amerika is er bij neuro-degeneratieve ziektes zoals Parkinson en Alzheimer een probleem met calcium ionen (Impaired calcium homeostasis).

Het biotech bedrijf doet nu onderzoek naar het eiwit Aequorin dat een calcium bindend eiwit is dat voorkomt in kwallen. Het doel is nu produkten te ontwikkelen die op basis van dit eiwit een oplossing zouden kunnen worden voor ziektes zoals Parkinson en Alzheimer.

The role of calcium in human physiology has been extensively researched throughout the last century. Disruptions in calcium homeostasis are known to cause and to correlate with a large number of diseases, syndromes and conditions. Following much investigation, calcium-binding proteins (CaBPs) have been recognized as protective factors in neuronal populations susceptible to toxicity via calcium and calcium-mediated actions. Aequorin is from the family of calcium-binding proteins known as the EF-hand family. Several CaBPs endogenous to the human body are also of the EF-hand family and have been found to serve protective roles in certain cellular populations. Quincy Bioscience intends to apply the technology developed from the aequorin molecule to develop products that fight neurodegenerative diseases such as Alzheimer's and Parkinson's diseases, by supplementing calcium binding proteins in an effort to restore calcium ion homeostasis.

Filmpje!
http://www.quincybioscience.com/videos/aequorin.mov

Website bedrijf
http://www.quincybioscience.com


Alzheimer Nederland

Nederland telt ongeveer 250.000 mensen met dementie. De belangrijkste en meest bekende oorzaak is de ziekte van Alzheimer. Bij mensen met dementie gaat het functioneren van de hersenen langzaam maar zeker achteruit. Zij worden in hun dagelijks leven steeds afhankelijker van de hulp van anderen. Een zorg die jaren achtereen, soms 24 uur per dag, wordt volgehouden. Alzheimer Nederland komt op voor de gezamenlijke belangen van mensen met dementie en hun familie en wijst de weg in het doolhof van de zorg bij dementie. Alzheimer Nederland stimuleert de overheid, verzekeraars en instellingen om de juiste voorzieningen te treffen en neemt waar nodig zelf initiatief. Door financiering van wetenschappelijk onderzoek hopen we dementie en de ernstige gevolgen zoveel mogelijk te voorkomen.

http://www.alzheimer-nederland.nl/


Internationale Stichting Alzheimer Onderzoek

De Internationale Stichting Alzheimer Onderzoek (ISAO) is een Nederlandse non-profit organisatie die tot doel heeft wetenschappelijk onderzoek naar de oorzaken van en de behandelingsmethoden voor de ziekte van Alzheimer en verwante vormen van dementie te ondersteunen en voorlichting te geven over de ziekte. De Stichting, die uitsluitend wordt ondersteund met giften van particulieren, is in november 1993 in Nederland opgericht. Sinds 1994 stelt de ISAO beurzen ter beschikking voor wetenschappelijk onderzoek naar de ziekte van Alzheimer en verwante vormen van dementie, met name voor fundamenteel en klinisch onderzoek. Met deze beurzen draagt de ISAO bij aan het vergroten van de kennis over de ziekte van Alzheimer. Daarnaast verstrekt de ISAO beurzen aan organisaties die van algemeen belang zijn voor het onderzoek naar de ziekte van Alzheimer, zoals weefselbanken. De ISAO ondersteunt alleen wetenschappelijk onderzoek dat wordt uitgevoerd door non-profit organisaties.

http://www.alzheimer.nl/


Wonen met dementie

"Wonen met dementie" is een werkprogramma dat kleinschalige zorg voor mensen met dementie wil stimuleren. Het richt zich op (toekomstige) cliënten, zorgorganisaties en woningcorporaties en kent drie hoofdlijnen, namelijk:

  • Informatie overdragen over wat kleinschalige zorg is, hoe het valt te realiseren en hoe het past in de plaatselijke en regionale situatie.
  • Ondersteunen van zorgorganisaties en woningcorporaties bij het ontwikkelen en realiseren van kleinschalige projecten. Verbindingen leggen met activiteiten van andere organisaties op het gebied van kleinschalige zorg en de aanwezige kennis bundelen en aanbieden.

http://www.wonenmetdementie.nl


Hoe herken ik Ziekte van Alzheimer

De ziekte is te herkennen aan voortschrijdende geestelijke achteruitgang, vaak het eerst tot uiting komend in geheugenstoornissen. Meer specifiek zijn de symptomen
• ernstige vergeetachtigheid
• desoriëntatie ten aanzien van plaats en tijd
• vermindering van de verstandelijke vermogens
• taalstoornissen
• persoonlijkheidsveranderingen
• stoornissen in de uitvoerende functies, zoals zelfzorg
• beperkingen in sociaal en beroepsmatig functioneren.

http://www.parnassia.nl


Alzheimercentrum

Het Alzheimercentrum binnen het VU medisch centrum is opgericht ten dienste van de patiëntenzorg en het patiëntgebonden wetenschappelijk onderzoek. Het Alzheimercentrum beoogt gecoördineerde en gestructureerde samenwerking binnen ziekenhuisafdelingen wat betreft de behandeling van de ziekte van Alzheimer en andere vormen van Dementie.

http://www.alzheimercentrum.nl/


Minder calorieën eten zou Alzheimer vertragen

Voeding die relatief weinig calorieën bevat, vermindert bij muizen de opstapeling van een stof die in verband wordt gebracht met geheugenverlies.

http://www.psycholoog.net/news.php?p1=viewcomment&which_article=740


Niet dement dankzij goed cholesterol

Alzheimer wordt vaak geassocieerd met bèta-amyloid plaques in de hersenen. Dat zijn een soort afzettingen van eiwit in de hersenen. “HDL, goed cholesterol,” vertelt de onderzoeker, “kan het vormen van deze plaques voorkomen. Bovendien werkt HDL ontstekingen tegen. Ontstekingen in de hersenen, die overigens vaak gepaard gaan met de plaques, kunnen ook leiden tot dementie. Dit zijn dus twee manieren waarop HDL tegen dementie zou kunnen beschermen.” Een paar manieren om je HDL-gehalte een klein beetje te verhogen zijn wel bekend. Alcohol drinken helpt wat, net als veel sporten en bewegen en een verhoging van de concentratie oestrogenen in het bloed (bij vrouwen). Overgewicht en roken verlagen de hoeveelheid HDL.

http://www.lumc.nl/1080/archief/2002/20020628.html


Ontspoorde hersenen

Er zijn families waarin Alzheimer al op middelbare leeftijd voorkomt. Soms worden daar mutaties in het gen voor APP (amyloid precursor protein) aangetroffen, het eiwit waaruit bèta-amyloïde ontstaat.

http://www.nrc.nl/W2/Nieuws/2000/12/30/Vp/wo.html


Rol van insuline bij Alzheimer

Brown Medical School (US) brengt insuline in het middelpunt van de belangstelling. Men vond abnormaal lage niveaus van insuline en insuline groeifactoren in delen van de hersenen die het meest waren aangetast door Alzheimer, en men vond dat deze lage niveaus bijdroegen tot “brain rotting”. Eerder onderzoek toonde aan dat insuline helpt bij het reguleren van amyloid en de vorming van destructieve vormen van tau helpt te voorkomen. Studies vonden tevens dat mensen met type 2 diabetes, waarbij de cellen ongevoelig worden voor insuline, een groter risico lopen op het ontwikkelen van Alzheimer.

http://www.hulporganisaties.be/Pages/details.asp?lng=NL&Id=1833


Vergeten en dan

Op de site vindt u gerangschikt in vier thema’s informatie over vergeetachtigheid en dementie. In het oerwoud van organisaties en instanties die u informatie en hulp kunnen bieden is het soms moeilijk de weg te vinden. Met deze website proberen wij u hierbij te helpen. U vindt hier een overzicht van de mogelijkheden die er zijn voor dementerenden en hun naasten, zoals: cursussen, hulp bij de dagelijkse bezigheden zoals het huishouden, mogelijkheden voor ontspanning, enzovoorts. Deze site is vooral bedoeld als een wegwijzer naar relevante organisaties en informatiebronnen. U zult dan ook merken dat u vaak wordt verwezen door middel van links en adressen. Bij het samenstellen van deze website is uitgegaan van het aanbod van niet-commerciële welzijns- en zorgorganisaties. Vooralsnog beperkt de informatie over aanbieders en instanties zich tot de volgende plaatsen in de provincie Utrecht: Utrecht (inclusief Vleuten-De Meern), Nieuwegein, Vianen, Lopik, IJsselstein en Houten.

http://www.vergetenendan.nl/


Ginkgo Biloba speelt een rol bij de remming van Alzheimer

ginkgo.jpg (92762 bytes) Professor Koji Nakanishi onderzoekt de rol van Ginkgo biloba en de eventuele mogelijkheden bij de ziekte van Alzheimer: Ginkgolides. Extracts of the "fossil tree" Ginkgo biloba are reputed to improve memory and sharpen mental alertness. This bioactivity has been attributed to the cage molecules ginkgolides. They act as potent antagonists of the platelet-activating factor receptor (PAFR, a GPCR).

Our aim is to study the neuromodulatory properties by determining the binding of ginkgolides to PAFR with cloned PAFR and in vivo and ex vivo studies of the central nervous system (CNS) by positron emission tomography (PET). Recently we have also found that gingkolides indeed prevent aggregation of the amyloid peptides that lead to Alzheimer’s disease.

Links


Lopende Alzheimer onderzoeken in Nederland

De volgende onderzoekers hebben geld ontvangen voor onderzoek
van de ISAO.

Onderzoeker: Dr. M. Gebbink
Instituut: Universiteit Medisch Centrum, Utrecht.
Afdeling: Haematologie.
Project: A novel Aß epitope as target of specific antibodies.
Duur: 01 November 2005 - 31 Oktober 2007.
Subsidie: € 60.000,-

Onderzoeker: Dr. B.N.M. van Berckel
Instituut: Vrije Universiteit Medisch Centrum, Amsterdam.
Afdeling Nuclear Medicine en PET Research.
Project: Imaging of amyloid in pre-symptomatic AD.
Duur: 01 November 2005 - 31 Oktober 2007.
Subsidie: € 80.000,-

Onderzoeker: Dr. W. Scheper
Instituut: Academisch Medisch Centrum, Amsterdam.
Afdeling: Neurogenetisch Laboratorium.
Project: Endoplasmatic reticulum stress in AD.
Duur: 01 November 2005 - 31 Oktober 2007.
subsidie: € 80.000,-

Onderzoeker: Dr. R.W.M.M. Jansen
Instituut: Nijmegen Medisch Centrum.
Afdeling: Geriatric Medicine.
Project: Cerebrovascular effects of cholinesterase inhibitors.
Duur: 01 November 2005 - 31 Oktober 2007.
Subsidie: € 80.000,-

Onderzoeker: Dr. M.I. Geerlings
Instituut: Universiteit Medisch Centrum, Utrecht.
Afdeling: Julius Centrum voor gezondheidswetenschappen en Eerstelijns Geneeskunde.
Project: Depression and AD: is stress the missing link?
Duur: 01 November 2005 - 31 Oktober 2007.
Subsidie: € 79.748,-

Onderzoeker: Dr. R. Lindeboom
Instituut: Academisch Medisch Centrum, Amsterdam.
Project: A test bank: efficient testing and screening for AD.
Duur: 01 November 2005 - 31 Oktober 2007.
Subsidie: € 80.000,-

Onderzoeker: Dr. E. van Someren
Instituut: Nederlands Instituut voor Hersenonderzoek en Vrije Universiteit Medisch Centrum.
Project: Can sleep therapy increase functional connectivity in early dementia?
Duur: 01 November 2005 - 31 Oktober 2007.
Subsidie: € 78.474,-

Onderzoeker: Dr. R. Verwer
Instituut: Nederlands Instituut voor Hersenonderzoek, Amsterdam.
Project: Functional activities of Alzheimer neurons.
Duur: 01 November 2005 - 31 Oktober 2007.
Subsidie: € 61.778,-

Dr. Wiep Scheper
Medisch Centrum Amsterdam, Neurogenetisch Laboratorium
Stress reactie van het endoplasmatisch reticulum bij de ziekte van Alzheimer
1 November 2005 - 30 oktober 2007

Een belangrijk kenmerk van de ziekte van Alzheimer is de ophoping van geaggregeerde eiwitten in de hersenen. Aß vormt het hoofdbestanddeel van deze plaques. Vooral in het endoplasmatische reticulum (ER) vindt de selectie van afwijkende eiwitten plaats. Wanneer dit systeem voor kwaliteitscontrole wordt overbelast, wordt er een stress reactie geactiveerd. Langdurige stress leidt tot het afsterven van cellen en vormt dus mogelijk een belangrijke factor in het neuronale verlies tijdens de progressie van Alzheimer.

Dr. Wiep Scheper en haar team hebben vastgesteld dat deze stress reactie van het ER wordt geactiveerd in de hersenen van Alzheimerpatiënten en dat deze reactie heftiger wordt naarmate de Aß-pathologie ernstiger is. Dit kan erop wijzen dat deze twee gebeurtenissen aan elkaar zijn gerelateerd. Om dit te kunnen testen, heeft het team experimenten met celculturen uitgevoerd. Hieruit bleek dat juist kleine Aß-aggregaten, die worden beschouwd als de echte boosdoeners voor Alzheimer, tot een activering van de stressreactie van het ER leiden in plaats van grote, volgroeide aggregaten.

Bovendien stelden zij een opvallende stijging van het gehalte van het eiwit Rab6A in de hersenen van Alzheimerpatiënten vast. Rab6A is mede verantwoordelijk voor het transport van eiwitten in cellen naar het ER. De onderzoekers konden een nauwe relatie tussen het Rab6A-gehalte en de stress reactie van het ER vaststellen. Scheper et al. veronderstellen dat de door Aß veroorzaakte stress reactie van het ER een belangrijke oorzaak voor neuronaal verlies bij Alzheimer vormt en dat dit wordt verergerd door de stressreactie van het ER op basis van een toegenomen transport naar het ER via Rab6A. Om deze reden willen zij de ER-stress reactie in relatie met de pathologische hoofdkenmerken van Alzheimer onderzoeken: Welke rol spelen Aß, neurofibrillaire veranderingen en het door Rab6A aangestuurde transport bij de stressreactie van het ER in relatie met de neurodegeneratie bij Alzheimer? Zij zullen gebruik maken van post-mortem hersenmateriaal, cellulaire modellen en in-vitro modellen voor Rab6A-aangestuurde transport.
Meer inzicht in de basismechanismen van de pathogenese is onmisbaar voor de ontwikkeling van diagnostische markers en vergroot de kans op een gerichte therapeutische interventie.

Dr. Martijn Gebbink

Afdeling hematologie,
Universitair Medisch Centrum Utrecht
Een nieuw Aß-epitoop als doelwit van specifieke antistoffen
1 November 2005 - 30 oktober 2007

) speelt een centrale rol in -peptide (A De aggregatie van amyloïde- de ziekte van Alzheimer. Daarom is er veel belangstelling voor de ontwikkeling worden ingezet, zorgen in van vaccins tegen Alzheimer. Antistoffen die tegen A theorie voor de omkering van de cognitieve achteruitgang en/of een effectieve verwijdering van amyloïdeafzettingen. Positieve resultaten na de vaccinatie van muizen wekten de hoop dat soortgelijke strategieën misschien ook bij mensen met Alzheimer werken. Het klinisch proefonderzoek werd echter abrupt stopgezet nadat bij ongeveer 5% van alle gevaccineerde patiënten ernstige bijwerkingen waren ontdekt, zoals ontstekingen van de hersenen.
Dit vormde een extra stimulans voor onderzoek naar het exacte . Er kwamen nieuwe inzichten werkingsmechanisme van de antistoffen tegen A beschikbaar, bijvoorbeeld dat diverse isotypen van antistoffen verschillende binden. reacties oproepen wanneer zij zich aan A
Er bestaat enig bewijs voor het feit dat de bijwerkingen die na de vaccinatie van Alzheimerpatiënten optraden, het resultaat zijn van een afwijkende auto-immuunreactie. Er dient echter verder te worden onderzocht of inderdaad de grondslag vormt voor deze problemen. Het auto-immuniteit tegen A immuunsysteem zou de ontsteking ook op een andere manier kunnen veroorzaken, namelijk via een overstimulatie van een regulerend systeem dat bekend staat als 'complement-activering'. Dit systeem speelt een rol bij de verdediging van de ontvanger.
Onlangs hebben Dr. Martijn Gebbink en zijn team een nieuw structureel aspect van Aß ontdekt - een specifiek herkenningspunt dat niet aanwezig is op het oplosbare peptide. Zij zijn erin geslaagd antistoffen van konijnen tegen dit nieuwe epitoop te ontwikkelen, de zogenoemde "cross-ß-structuur". Er zijn sterke aanwijzingen dat de antistoffen zich aan een structurele bouwsteen binden die niet alleen in Aß-fibrillen aanwezig is, maar in elk willekeurig polypeptide die een amyloïdestructuur heeft aangenomen. Dit is een nieuwe ontdekking dat de deur opent naar nieuwe manieren om de exacte interactie tussen antistoffen en geaggregeerd Aß te onderzoeken. Naar aanleiding van deze nieuwe gegevens veronderstellen Gebbink et al. dat het structurele epitoop een nieuw en nog niet eerder ontdekt structureel antigen biedt voor de ontwikkeling van nieuwe reagenten in de strijd tegen de fibrillen. Dit willen zij via deze studie onderzoeken.
Gebbink et al. zullen specifieke antistoffen selecteren die Aß-fibrillogenese tegengaan en het toxische effect van Aß op cellen voorkomen, onafhankelijk van het immuunsysteem. Vervolgens zullen zij het minimale fragment van de antistoffen definiëren dat de Aß-pathologie kan omkeren. Men kan ervan uitgaan dat dit minimale actieve fragment geen delen meer bevat van de antistoffen die een immuunreactie oproepen. Op deze manier zullen er minder snel ontstekingsreacties ontstaan wanneer de fragmenten worden toegediend.

Dr. Ronald Verwer

Nederlands Instituut voor Hersenonderzoek
Functionele activiteiten van Alzheimer-neuronen
1 November 2005 - 30 oktober 2007

Een verminderde metabolische activiteit en atrofie van neuronen zijn belangrijke kenmerken van de ziekte van Alzheimer. Gezien het feit dat veel neuronen in de meeste delen van de hersenen nog steeds aanwezig zijn bij Alzheimerpatiënten, zij het in een minder actieve vorm, lijkt een reactivering van deze neuronen een veelbelovende therapeutische strategie voor Alzheimer. Dr. Ronald Verwer en zijn team hebben een in-vitro systeem van postmortaal menselijk hersenweefsel ontwikkeld om de functionele activering van neuronen tijdens het verouderingsproces en Alzheimer te bestuderen. Neuronen die zijn verkregen via vroegtijdige autopsies blijven nog gedurende enkele weken in leven en kunnen tijdens experimenten worden gemanipuleerd.

Verwer et al. hebben aangetoond dat neurotrofische factoren de levensvatbaarheid van de cellen in de op kweek gezette postmortale plakjes kunnen verbeteren. Andere onderzoekers hebben aangetoond dat zenuwgroeifactor leeftijdsgerelateerde neuronale atrofie bij apen kan omkeren. Verwer en zijn team hebben onlangs ook vastgesteld dat de elektrofysiologische activiteit van cellen in postmortale plakjes hoger is wanneer neurotrofische factoren aan het medium worden toegevoegd. Zij willen de functionele activiteit van neuronen in op kweek gezette plakjes van Alzheimerpatiënten correleren met de mate van de Alzheimerpathologie.
Neurale stam-/precursorcellen vormen de meest veelbelovende manier om verloren neuronen te vervangen en in een beschadigd neuronaal netwerk te integreren ter bevordering van een functioneel herstel. Uit diverse studies blijkt echter dat neurale precursorcellen in veel hersendelen van volwassenen kunnen voorkomen en dat neurale precursorcellen bij dieren niet zozeer de verloren neuronen vervangen, maar eerder degenererende neuronen redden.

De op kweek gezette culturen van postmortaal hersenweefsel bieden een uniek systeem om de gecombineerde effecten te bestuderen van neurotrofische factoren en de factoren van neurale stamcellen op de functionele activiteit van Alzheimer-neuronen. Verwer en zijn team gaan ervan uit dat de functionele activiteit van neuronen van oudere, gezonde proefpersonen en Alzheimerpatiënten door neurotrofische factoren en factoren van neurale stamcellen kan worden gestimuleerd. Met deze studie wil Verwer de functionele activiteit van neuronen in postmortaal hersenweefsel van Alzheimerpatiënten en controlemonsters van oudere proefpersonen beschrijven in relatie tot neurotrofische factoren en neurale stamcellen.

Het doel op lange termijn is de ontwikkeling van strategieën voor een reactivering van geatrofieerde en gedegenereerde neuronen om het ziekteverloop van Alzheimer om te keren.

Bart van Berckel

Department of Nuclear Medicine & PET research
VU University Medical Centre
Imaging van amyloïde in het presymptomatische stadium van Alzheimer
1 November 2005 - 30 oktober 2007

De ziekte van Alzheimer is een fatale stoornis van de hersenen. Alzheimer wordt gekenmerkt door een progressieve verslechtering van het vermogen dagelijkse activiteiten uit te voeren, een vermindering van de cognitieve functies, zoals geheugenfuncties, en diverse psychiatrische symptomen en gedragsstoornissen. De diagnose van Alzheimer is voornamelijk gebaseerd op de herkenning van deze klinische symptomen en is alleen betrouwbaar wanneer de ziekte al ver gevorderd is. Het is erg moeilijk om een diagnose te stellen in de beginfase van de ziekte, wanneer alleen subtiele en beperkte symptomen aanwezig zijn die niet specifiek zijn voor de aandoening. Er bestaat daarom een grote behoefte aan een methode om Alzheimer al in een vroegtijdige fase te kunnen diagnosticeren.

De ziekte van Alzheimer wordt gekenmerkt door abnormale afzettingen van het proteïne beta-amyloïde (Aß) in de hersenen. Tot voor kort konden deze afwijkende afzettingen alleen in beeld worden gebracht door een microscopische analyse van de hersenen na het overlijden van de patiënt. De aanwezigheid van deze Aß-afzettingen is feitelijk noodzakelijk om de uiteindelijke diagnose voor Alzheimer te kunnen stellen. Door veel onderzoekers wordt aangenomen dat Aß al gedurende lange tijd in de hersenen aanwezig is, voordat zich de ziekte van Alzheimer openbaart. Om deze reden is een vroegtijdige ontdekking van pathologische Aß-ophopingen van groot belang. Hiermee kunnen personen met een risico op Alzheimer immers worden geïdentificeerd.

Via neuroimaging-technieken zoals Positron Emissie Tomografie (PET) is in-vivo beeldvormend onderzoek en een kwantificering van de amyloïdeophopingen in de hersenen mogelijk. Dit is een heel nieuwe toepassing van de PET-techniek. Onlangs werden enkele PET-tracers ([18F]FDDNP en [11C]PIB) voor dit doel ontwikkeld en de eerste klinische studies met Alzheimerpatiënten zijn veelbelovend. Voor beide tracers dienen nog talrijke methodologische kwesties te worden opgelost en de klinische waarde van in-vivo beeldvormend onderzoek van amyloïde moet nog worden bevestigd.

Met dit project worden twee doelen nagestreefd: het bieden van een onafhankelijke en onbevooroordeelde evaluatie van de waarde van amyloïde-imaging voor de (vroegtijdige) diagnose van Alzheimer en de optimalisering van methoden voor de kwantificering van de amyloïdeophopingen in de hersenen.

Dr. Eus van Someren

Nederlands Instituut voor Hersenonderzoek en VU medisch centrum Amsterdam
Kan slaaptherapie de functionele connectiviteit bij vroegtijdige dementie verbeteren?
1 November 2005 - 30 oktober 2007

In de beginfase van de ziekte van Alzheimer is het meest kenmerkende cognitieve probleem een verminderd geheugen voor feiten en gebeurtenissen, gevolgd door problemen bij ingewikkelde taken. Uit neuroimaging-onderzoek blijkt dat bepaalde delen en verbindingen in de hersenen mogelijk actief worden om de functies van de door de ziekte aangetaste gebieden over te nemen en deze cognitieve problemen te compenseren. De mogelijkheid dergelijke compenserende hersenmechanismen te activeren om geheugenproblemen tegen te gaan, vormt mogelijk het cruciale verschil tussen een redelijke kwaliteit van leven en volledige hulpbehoevendheid.

Interessant genoeg kunnen de boven genoemde cognitieve problemen uit de beginfase van Alzheimer - problemen bij het onthouden van feiten en gebeurtenissen en de uitvoering van complexe taken - ook ontstaan bij gezonde proefpersonen indien hen slaap wordt ontzegd. Gezien het feit dat veel ouderen en erg veel Alzheimerpatiënten aan slaapproblemen lijden, is het goed mogelijk dat hun cognitieve problemen worden verergerd door een slechte nachtrust.

Dr. Eus van Someren veronderstelt dat de problemen van patiënten met een milde vorm van Alzheimer door een slechte nachtrust worden verergerd. Een slaaptekort kan de compenserende activiteit van - met name prefrontale - gebieden en verbindingen in de hersenen belemmeren. Deze mechanismen worden met behulp van hersenscans onderzocht. Van Someren et al. willen een goede nachtrust bevorderen en verwachten dat de compenserende mechanismen in de hersenen hierdoor gedeeltelijk kunnen worden verbeterd en tot optimale cognitieve prestaties kunnen leiden binnen de beperkingen van de ziekte. Indien hij succesvol blijkt te zijn, kan een uitgebreidere toepassing van slaapstimulerende methoden tot een verbeterde levenskwaliteit van Alzheimerpatiënten leiden.

Dr. Mirjam Geerlings

Universitair Medisch Centrum Utrecht
Julius Centrum voor Gezondheidswetenschappen en Eerstelijns Geneeskunde,
Depressie en de ziekte van Alzheimer: vormt stress de ontbrekende schakel?
1 November 2005 - 30 oktober 2007

Er bestaat toenemende belangstelling voor de mogelijke rol van depressie en stresshormonen als risicofactoren voor de ziekte van Alzheimer. Stresshormonen, zoals cortisol, zouden een rol kunnen spelen in de relatie tussen depressies en het risico op de ziekte van Alzheimer. Personen met een depressie hebben in veel gevallen een verhoogde afgifte van cortisol. Ernstige of chronische stress zou schade kunnen toebrengen aan de hippocampus, een hersenstructuur van belang voor de geheugenfunctie en die in een vroeg stadium van de ziekte van Alzheimer is aangetast. Uit dierproeven blijkt een mogelijke direct biologisch effect van stresshormonen op de hippocampus. Het is echter nog niet duidelijk of stress bij mensen tot de ziekte van Alzheimer kan leiden.

Dr. Mirjam Geerlings en haar team veronderstellen dat een verhoogd cortisolgehalte en een langdurige blootstelling aan psychosociale stress risicofactoren vormen voor atrofie van de hippocampus en cognitieve achteruitgang. Zij nemen aan dat een depressie op latere leeftijd in wisselwerking staat met deze factoren en zo tot atrofie van de hippocampus en cognitieve achteruitgang kan leiden.

Zij zullen dit in de vorm van een prospectieve cohortstudie onderzoeken. De groep proefpersonen zal bestaan uit 1704 personen, in de leeftijd van 55-85 jaar op baseline van het Longitudinaal onderzoek zelfstandigheid van ouderen (LASA) en 841 patiënten in de leeftijd 50 jaar en ouder van het onderzoek Second Manifestation of ARTerial disease study (SMART). Depressie wordt op een symptomatisch en diagnostisch niveau onderzocht; psychosociale stress wordt vastgesteld met ingrijpende gebeurtenissen in de vroege en late levensfase, en stresshormonen met serum cortisol en de 24-uurs cortisoluitscheiding in speeksel.

Het is van essentieel belang om risicofactoren van Alzheimer te identificeren, voordat de ziekte zich klinisch openbaart indien behandelingsstrategieën ter voorkoming of vertraging van de ziekte een kans van slagen willen hebben. Deze studie kan een belangrijke rol spelen bij de voorkoming of vertraging van de progressie van de ziekte van Alzheimer.

Dr. René Jansen

Universitair Medisch Centrum Radboud Nijmegen,
afdeling Geriatrie
Cerebrovasculaire effecten van cholinesteraseremmers
1 April 2006 - 31 maart 2008

De zogenoemde cholinesteraseremmers, donepezil, rivastigmine (Exelon) en galantamine (Reminyl) - zijn medicijnen die voor de behandeling van de ziekte van Alzheimer worden ingezet. Dr. René Jansen en zijn team hebben reden te geloven dat de werking van deze geneesmiddelen verschilt van wat tot nu toe werd aangenomen. Zij veronderstellen dat cholinesteraseremmers de bloedtoevoer naar de hersenen kunnen verbeteren door de stimulering van zenuwen die de bloedvaten naar de hersenen reguleren. Hierdoor zou de hersenfunctie verbeteren, waardoor ook het zelfstandig functioneren van Alzheimerpatiënten vooruitgaat. Hierdoor zouden ook verdere hersenbeschadigingen kunnen worden voorkomen of vertraagd.

Veel Alzheimerpatiënten vertonen bovendien tekenen van vasculaire aandoeningen in hun hersenen, die cognitieve en functionele problemen in de hand werken. Een verbeterde bloedtoevoer naar de hersenen zou de effecten van vasculaire aandoeningen gedeeltelijk kunnen tegengaan.
In deze studie hebben Jansen et al. vier specifieke doelen opgesteld waarmee zij deze hypothese willen onderbouwen: 1) Zij zullen onderzoeken of de behandeling met een cholinesteraseremmer de bloedtoevoer naar de hersenen verbetert. 2) Zij zullen testen of deze medicijnen de hersenen kunnen helpen om een voldoende grote bloedstroom te handhaven ook al varieert de bloeddruk. 3) Zij zullen onderzoeken of de progressie van cerebrovasculaire schade bij Alzheimerpatiënten met deze behandeling kan worden vertraagd en of dit is gerelateerd aan een relevant voordeel voor deze patiënten. 4) Zij zullen zoeken naar een effect op de bloedstroom naar de hersenen in de beginfase van de behandeling om te kunnen testen of hiermee verbeteringen bij een langdurige behandeling van de patiënt mogelijk zijn.

Er zal een willekeurige klinische, placebogecontroleerde studie worden uitgevoerd onder 80 patiënten die aan een milde tot gematigde vorm van Alzheimer lijden. De effecten op de bloedtoevoer naar de hersenen en de cerebrovasculaire schade zullen met behulp van geavanceerde technieken worden onderzocht: transcraniële dopplersonografie (TCD), nabij-infrarood spectroscopie (NIRS), fasecontrast magnetische resonantie imaging en diffusie tensor imaging (DTI). De cognitieve resultaten worden via neuropsychologische tests geëvalueerd. Hiertoe behoren ook evaluaties van de aandachtsfunctie en uitvoerende functies. Uit de resultaten van deze uiterst belangrijke studie moet blijken of via een behandeling met deze medicijnen beginnende of nieuwe hersenbeschadigingen kunnen worden verminderd. Men wil bovendien vaststellen of een verbeterde bloedtoevoer naar de hersenen in verband staat met een verbetering van het klinisch functioneren.

Dr. Robert Lindeboom

Academisch Medisch Centrum Amsterdam
Efficiënt testen van en screenen op Alzheimer via een itembank
1 November 2005 - 30 oktober 2007

Neuropsychologisch testen van en screenen op Alzheimer is tijdrovend en belastend voor de patiënt. Bovendien is de diagnostische waarde van de tests beperkt, vooral in de beginfase van Alzheimer, waardoor de ziekte veelal laat wordt opgemerkt.

Met dit project willen de onderzoekers een itembank ontwikkelen en kalibreren voor het efficiënt testen en screenen van de ziekte van Alzheimer. Een gekalibreerde itembank is een uitgebreide verzameling van neuropsychologische testvragen waarvan de meeteigenschappen (moeilijkheid, differentiatie) bekend zijn. Het kalibreren van de itembank gebeurt via statistische analyses uit de item-respons-theorie (IRT). Het doel is alle items van de itembank op één algemene moeilijkheidsschaal te brengen waarbij de log-odds als meeteenheid wordt gehanteerd. Een gekalibreerde itembank kan worden gebruikt om proefpersonen via een CAT-procedure (computer-adaptieve test) te testen. Door de inzet van CAT denken Dr. Robert Lindeboom en zijn team de testbelasting met 70% te kunnen verlagen, zonder enig nauwkeurigheidsverlies. Bovendien kunnen uit de itembank Alzheimer-specifieke testvragen worden geselecteerd voor een verbeterde screening van de ziekte. Ook kunnen gebruikers van de itembank hun resultaten met elkaar vergelijken, zelfs als ze verschillende vragen hebben gebruikt.

Ten slotte worden zowel de testvragen als de proefpersonen met dezelfde log-odds eenheid schaal gemeten en kunnen scores worden omgezet in een kans op een correct antwoord voor elke testvraag. Lindeboom et al. verwachten dat de conversie van ruwe testscores (bijvoorbeeld "2 punten" op de ADAS-Cog) naar log-odds tot een eenvoudiger interpretatie van cognitieve veranderingen in patiënten leidt dan tot nu mogelijk was.
Samengevat, via de ontwikkeling van een IRT-gekalibreerde itembank willen Lindeboom en zijn groep:

- De testbelasting voor personen met geheugenklachten aanzienlijk verminderen
- Vroegtijdiger herkenning van proefpersonen die vermoedelijk aan Alzheimer lijden.
- Verbeterde uitwisseling van onderzoeksresultaten.
- Eenvoudiger interpretatie van testresultaten door toepassing van een formele epidemiologische meeteenheid, de log-odds, wat nuttig kan zijn bij therapeutische beslissingen.


Milieuverontreiniging en neurodegeneratieve dementie

Een literatuurstudie naar milieuvervuiling als mogelijke risicofactor voor versnelde veroudering en progressieve neurodegeneratieve aandoeningen.

http://www.rug.nl/wewi/_shared/publicaties/biologie/rap62.pdf?as=text


Internationaal



Can an omega-3 fatty acid slow the progression of Alzheimer's disease?

Nutritionists have long endorsed fish as part of a heart-healthy diet. Some studies suggest that omega-3 fatty acids found in the oil of certain fish may also benefit the brain by lowering the risk of Alzheimer's disease. In order to test whether an omega-3 fatty acid can impact the progression of Alzheimer's disease, researchers supported by the National Institute on Aging will evaluate one in a clinical trial.

http://www.nia.nih.gov/NewsAndEvents/PressReleases/PR20070510DHAStudy.htm



Foie gras could be tasty way to get Alzheimer’s

FOIE GRAS, enjoyed as a luxury since ancient Egyptian times, may be linked to the onset of diseases including Alzheimer’s, type 2 diabetes and rheumatoid arthritis, researchers have suggested.

http://www.timesonline.co.uk/tol/news/uk/health/article1942949.ece



Emotional Stress Could Be a Factor in Causing Alzheimer’s

From the political to the science, Chinese medicine is a debated concept in Western society. However, this is a beginning to evaluating the theories that have been applied and experimented with over time. Through the different systems of Chinese medicine to the constant use by individuals who are looking for holistic health, Chinese medicine continues to become significant in Western society.

http://www.medindia.net/news/Emotional-Stress-Could-Be-a-
Factor-in-Causing-Alzheimers-Study-22155-1.htm



Blocking stress protein decreases Alzheimer's peptide in mice

Scientists revealed in November 2006 that stress increases production in mice of a brain peptide critical to Alzheimer's disease. Now the same group has shown that blocking a different brain peptide slows the stress-induced increase, opening a new door to treatment. Researchers from Washington University School of Medicine in St. Louis report the results online this week in the Proceedings of the National Academy of Sciences.

http://mednews.wustl.edu/news/page/normal/9576.html



Can An Omega-3 Fatty Acid Slow The Progression Of Alzheimer's Disease?

In order to test whether docosahexaenoic acid (DHA), an omega-3 fatty acid, can impact the progression of Alzheimer's disease, researchers at Washington University School of Medicine and Saint Louis University School of Medicine will evaluate DHA in a clinical trial sponsored by the National Institute on Aging (NIA).

http://www.sciencedaily.com/releases/2007/04/070402230158.htm



Omega-3 Fatty Acid Trial to Study Effect on Progression of Alzheimer

Nutritionists have long endorsed fish as part of a heart-healthy diet, and now some studies suggest that omega-3 fatty acids found in the oil of certain fish and algae could lower the risk of Alzheimer’s disease. Researchers at the University of Rochester Medical Center will take part in a national clinical trial of one omega-3 fatty acid, docosahexaenoic acid (DHA), to determine its impact, if any, on the progression of Alzheimer’s disease. The trial is supported by the National Institute on Aging (NIA).

http://www.urmc.rochester.edu/pr/news/story.cfm?id=1468



Cloned pigs help scientists towards a breakthrough in Alzheimer's

The first pigs containing genes responsible for Alzheimer’s disease will be born in Denmark in August. This event is a landmark achivement in the effort towards finding a cure for the disease. Scientists from the universities of Copenhagen and Århus, Denmark are once again at the cutting edge of biotechnology. This time with cloned pigs that have been genetically modified so that they may function as animal models for the notorious Alzheimer’s disease. In the US alone, 5 million people suffer from this human brain disorder and globally the number is set at approx. 24 million

http://www.ku.dk/english/news/?content=http://www.ku.dk/english/news/alzheimer.htm



Mechanism of nicotine's learning effects explored

While nicotine is highly addictive, researchers have also shown the drug to enhance learning and memory -- a property that has launched efforts to develop nicotine-like drugs to treat cognitive deficits in Alzheimer's and Parkinson's diseases, schizophrenia and attention-deficit/hyperactivity disorder.

http://www.eurekalert.org/pub_releases/2007-04/cp-mon033007.php



Study shows hope for early diagnosis of Alzheimer's

Electroencephalograms can help in the diagnosis of early-stage Alzheimer's disease, indicates a multi-year study by three institutions for the National Institutes of Health's National Institute on Aging.

http://www.rowan.edu/news/display_article.cfm?ArticleID=1753



Alzheimer’s prevention role discovered for prions

A role for prion proteins, the much debated agents of mad cow disease and vCJD, has been identified. It appears that the normal prions produced by the body help to prevent the plaques that build up in the brain to cause Alzheimer’s disease. The possible function for the mysterious proteins was discovered by a team of scientists led by Medical Research Council funded scientist Professor Nigel Hooper of the University of Leeds. Alzheimer’s and diseases like variant Creutzfeldt-Jakob Disease follow similar patterns of disease progression and in some forms of prion disease share genetic features. These parallels prompted Professor Hooper’s team to look for a link between the different conditions. They found an apparent role for normal prion proteins in preventing Alzheimer’s disease.

http://www.alphagalileo.org/index.cfm?fuseaction=readrelease&releaseid=521675&ez_search=1



Immune antibodies penetrate neurons to clear Alzheimer's-linked amyloid

Researchers at Weill Cornell Medical College have gotten much closer to understanding how immune-based therapies can treat Alzheimer's disease -- by studying how antibodies go inside brain cells to reduce levels of Alzheimer's-linked amyloid peptides that form plaques between neurons.

http://news.med.cornell.edu/wcmc/wcmc_2007/05_22_07.shtml



Diabetes may be associated with increased risk of mild cognitive impairment

Individuals with diabetes may have a higher risk of developing mild cognitive impairment, a condition that involves difficulties with thinking and learning and may be an intermediate step toward Alzheimer's disease.

http://www.eurekalert.org/pub_releases/2007-04/jaaj-dmb040507.php



Turning off gene makes mice smarter

Turning off a gene that has been associated with Alzheimer's disease made mice smarter in the lab, researchers said on Sunday in a finding that lends new insight on learning and may lead to new drugs for memory problems.

http://www.reuters.com/article/healthNews/idUSN2546860920070527



Research could lead to treatment for Alzheimer's disease

A molecule designed by a Purdue University researcher could lead to the first drug treatment for Alzheimer's disease. "There are many people suffering, and no effective treatment is available to them," said Arun Ghosh, the Purdue professor who designed the molecule. "There is an urgent need for a drug to treat this devastating disease, and the scientific community has been working on this problem for many years."

http://news.uns.purdue.edu/x/2007a/070417GhoshAlzheimers.html



Omega-3 fatty acid may help prevent Alzheimer's brain lesions

A type of omega-3 fatty acid may slow the growth of two brain lesions that are hallmarks of Alzheimer's disease, UC Irvine scientists have discovered. The finding suggests that diets rich in docosahexaenoic acid (DHA) can help prevent the development of Alzheimer's disease later in life.

http://today.uci.edu/news/release_detail.asp?key=1594



Celera Identifies Novel Genes Associated with Late-Onset Alzheimer’s Disease

Celera (NYSE: CRA), an Applera Corporation business, today announced the publication of data from its research studies identifying several candidate genetic markers associated with late-onset Alzheimer’s disease (LOAD), including markers in multiple genes that have never been associated with LOAD. Two of these genes are PCK1, a gene that regulates blood glucose levels, and GALP, a gene that is modulated by insulin and regulates food intake, suggesting a link between Alzheimer’s disease and irregular glucose/insulin levels.

http://home.businesswire.com/portal/site/google/index.jsp?ndmViewId
=news_view&newsId=20070227005346&newsLang=en



Martek's DHA algal oil reduces brain lesions in Alzheimer's animal model

This pre-clinical study conducted at the University of California Irvine, with Martek support, used genetically modified mice. It is the first study to show that docosahexaenoic acid (DHA), an omega-3 fatty acid, may slow the accumulation of a protein, tau, that leads to the development of neurofibrillary tangles, one of two signature brain lesions of Alzheimer's disease. Confirming previous research, DHA also was found to reduce levels of another protein, beta amyloid, which can clump in the brain and form plaques, the other Alzheimer's lesion. Previous work has shown that DHA may have therapeutic value for Alzheimer's patients. This pre- clinical research is among the first to show that DHA may play a role in delaying the onset of the disease.

http://www.news-medical.net/?id=23800



Early Results Indicate Pain Medications Don’t Prevent Alzheimer’s

Neither the over-the-counter pain medication naproxen nor the prescription pain reliever celecoxib appears to help prevent Alzheimer’s disease, according to the early results of a study published April 25 in the online edition of Neurology, the scientific journal of the American Academy of Neurology.

http://www.urmc.rochester.edu/pr/news/story.cfm?id=1447



Researchers Find Ways to Reduce Side Effects in the Treatment of Damaging Protein Plaques

When protein plaque builds up in the blood, it can result in serious diseases such as heart disease and Alzheimer's. Cyclooxygenase (COX) inhibitors, a class of drugs under investigation for the treatment of one cause of plaque build-up, also exhibit negative side effects.

Researchers in the International Institute of Nano and Molecular Medicine at the University of Missouri-Columbia are studying the possible use of carboranes, which are clusters of boron and carbon atoms, to prevent such side effects. These boron-rich clusters are substituted for carbon-based benzene rings commonly found in pharmaceuticals of all types, including COX inhibitors, which give unwanted side effects.

COX activity is seen in common nonsteroidal anti-inflammatory drugs like aspirin and ibuprofen. However, prolonged use of COX inhibitors can result in a variety of negative side effects, such as possible digestive and liver problems. Some COX inhibitors have recently been pulled from the market due to an increased risk of heart complications.

http://munews.missouri.edu/NewsBureauSingleNews.cfm?newsid=14788



Cortex area thinner in youth with Alzheimer's-related gene

A part of the brain first affected by Alzheimer's disease is thinner in youth with a risk gene for the disorder, a brain imaging study has found. A thinner entorhinal cortex may render these youth more susceptible to degenerative changes and mental decline later in life. This learning and memory hub is thinner in youth with the Alzheimer's-releated ApoE4 variant of the apolipoprotein gene, perhaps lowering the threshold for adverse consequences with aging-related tissue loss.

http://www.nimh.nih.gov/press/alzheimerscortex.cfm



Movement of new cells pave way for brain research

Research from The University of Auckland, alongside colleagues in Sweden, has identified how stem cells, immature cells that have not yet developed specific specialised functions, move from the site of generation in the brain, to other areas including those affected by neurological diseases. “We’ve known about the migration of brain cells in mammals for some years but humans have usually been deemed different,” says Professor Richard Faull of the University’s Faculty of Medical and Health Sciences. “Our studies show that stem cells migrate long distances through the human brain in order to replace cells that die in the olfactory system. Utilisation of this migration may allow us to direct the stem cells to other brain regions that are affected by brain cell loss. In addition, our study looked at adult brain tissue, which means much of the brain’s ability to regenerate remains active even in older human brains. “This research will change the way in which we can look at diseases where brain cells die, such as Huntington’s Disease, or require repair, such as stroke. By knowing how stem cells move around, we can now look at new ways to regenerate cells and repair damage to the areas of the brain affected by these conditions.”

http://www.health.auckland.ac.nz/news-events/news.html?id=407&from=more



Alzheimer's Study Has Innovative Approach

A U.S. scientist says the true cause of the neurological damage resulting from Alzheimer's disease might rest in the way certain brain proteins fold. Professor Michael Bowers of the University of California-Santa Barbara says the key to his approach is understanding the way those proteins fold, or rather, "misfold."

http://www.playfuls.com/news_004739_Alzheimers_Study_Has_Innovative_Approach.html



Protein inhibitor tangles with Alzheimer's disease

Mayo Clinic researchers have now shown that a drug that inhibits the function of the protein Hsp90 reduces brain levels in mice of the protein tau, the abnormal accumulation of which has been implicated in the pathogenesis of Alzheimer’s disease (AD). The study appears online on February 15 in advance of publication in the March print issue of the Journal of Clinical Investigation. A hallmark of AD is the abnormal accumulation of phosphorylated tau (p-tau) proteins resulting in the formation of neurofibrillary tangles, which impair the function of brain axons. Enhancing the removal of these p-tau proteins may therefore be a relevant therapeutic strategy. In the current study, Leonard Petrucelli and colleagues from the Mayo Clinic showed that a complex of two proteins, CHIP and Hsp90 (which are involved in protein refolding and degradation), plays a role in alleviating p-tau accumulation in mice and cultured human cells. They went on to show that administration of an Hsp90 inhibitor, EC102, to mice overexpressing human tau caused a significant reduction in p-tau levels. The findings point to a pivotal role for Hsp90 in aberrant tau degradation and potentially in tau refolding. Unlike many drugs, EC102 is able to cross the blood-brain barrier, making it a highly promising therapeutic candidate for AD and other conditions in which tau accumulates in abnormally high levels in the brain.

http://www.eurekalert.org/pub_releases/2007-02/joci-pit020807.php



Study examines genetic risk factors for Alzheimer's disease

Cardiff University researchers have found evidence for new genes involved in the development of Alzheimer’s disease.

The study, to be published in the next issue of the journal Human Molecular Genetics, tested more than 17,000 gene variants in 4,000 volunteers.

Several genes were found to show evidence of contributing to Alzheimer’ disease, the most interesting gene being ‘GALP’ which could affect the development of tangles within brain cells, a hallmark of Alzheimer’s disease.

Professor Julie Williams, School of Medicine, who leads this project with Professor Micheal Owen said: “Whilst these genes are likely to make modest contributions to disease more work needs to be done to test their strength in other samples of volunteers.”

Professor Owen, School of Medicine said: “Identifying susceptibility genes for Alzheimer’s disease provides a knowledge base for the development of potential new treatments and diagnostic tests. This study is just the first in series we are undertaking using new technology to look comprehensively at every gene in the human genome in Alzheimer’s Disease and we hope that there are other exciting findings to come.”

There is no known cure or preventative treatment for Alzheimer’s disease, which affects one in 20 people over the age of 65 and one in five over the age of 80 in the UK and more than 12 million people worldwide. The disease causes a distressing, irreversible and progressive loss of brain function and memory.

The School of Medicine’s Department of Psychological Medicine has established a bank of more than 3,000 volunteers in South Wales, and elsewhere in the UK, to identify possible genetic risk factors for Alzheimer's Disease.

"This is one of the largest studies of its kind and involves many Welsh families " said Professor Julie Williams. “It is by virtue of the support given to us by Alzheimer's sufferers and their carers that we are able to understand factors involved in the disease process. Many genes will be linked with Alzheimer’s disease and our current programme of research is designed to identify them.”

http://www.eurekalert.org/pub_releases/2007-03/cu-seg030507.php



Common enzyme interaction could hold clues to Alzheimer’s

McGill University researchers have identified a key two-part process in normal brain development that could shed new light on what causes some people to develop Alzheimer’s disease. Their findings appear in the March issue of Journal of Biological Chemistry.

Dr. Hemant Paudel, an associate professor of medicine at McGill and Alzheimer’s researcher at the Lady Davis Institute for Medical Research at the Jewish General Hospital, led a three-person team that used gene-modified mice and brain cell cultures in search of clues to the origins of Alzheimer’s.

They found that an enzyme called cyclin-dependent protein kinase 5 inhibits the activity of another enzyme called protein phosphatase 1. Both enzymes contribute to the functioning of the so-called tau protein. Tau protein has the potential to cause neuropathological tangles observed post-mortem in the brains of patients who had Alzheimer’s disease.

“Because one enzyme blocks the other, it’s similar to when a ruptured water pipe leaks into a basement with a blocked drain,” explained Dr. Paudel. “This raises questions such as, ‘Can we close the tap and unblock the drain – or, in the case of our research, can we induce tangles in the cell and if so, can we stop them from developing?’”

http://www.mcgill.ca/newsroom/news/?ItemID=24110



Study confirms imaging compound identifies amyloid-beta in human brain

A team led by Massachusetts General Hospital investigators has confirmed that the imaging agent Pittsburgh Compound B (PiB) binds to the protein in amyloid plaques that characterize Alzheimer's disease in the human brain. Their report describes the first postmortem neuropathological study of a dementia patient who had previously participated in a PET imaging study using PiB.

http://www.eurekalert.org/pub_releases/2007-03/mgh-sci030707.php



Scientists Identify 'Missing Link' in Process Leading to Alzheimer's Disease

Scientists at the University of Virginia have identified what appears to be a major missing link in the process that destroys nerve cells in Alzheimer’s disease, an incurable disease that slowly destroys memory and cognitive abilities. The findings are reported in the Nov. 20, 2006, issue of the Journal of Cell Biology and could eventually lead to new drugs that target and disrupt specific proteins that conspire in the brain to cause Alzheimer’s. In Alzheimer’s disease, two kinds of abnormal structures accumulate in the brain: amyloid plaques and neurofibrillary tangles. The plaques contain fibrils that are made from protein fragments called “beta-amyloid peptides.” The tangles also are fibrous, but they are made from a different substance, a protein called “tau.” In the new U.Va. study, the researchers found a deadly connection between beta-amyloid and tau, one that occurs before they form plaques and tangles, respectively. According to George Bloom, the senior author of the study and a professor of biology and cell biology at U.Va., this connection causes the swiftest, most sensitive and most dramatic toxic effect of beta-amyloid found so far. What makes it most remarkable, though, is that it requires a form of amyloid that represents the building blocks of plaques, so called “pre-fibrillar beta-amyloid,” and it only happens in cells that contain tau. Even though they account for just ~10 percent of the cells in the brain, nerve cells are the major source of tau, which likely explains why they are specifically attacked in Alzheimer’s disease.

http://www.virginia.edu/uvatoday/newsRelease.php?print=1&id=1435



Evidence of a Role for Lactadherin in Alzheimer’s Disease

In conclusion, lactadherin plays an important role in the phagocytosis of Aß 1-42 peptide, and its expression is reduced in Alzheimer’s disease. Alterations in lactadherin production/function may contribute to the initiation and/or progression of Alzheimer’s disease.

http://ajp.amjpathol.org/cgi/content/abstract/170/3/921



Grape and Berry Juices - Elixers for Long Life?

According to a new study by scientists at the University of Glasgow in Scotland, purple grape juice is now your best bet for preventing heart disease, Alzheimer's disease and a host of other chronic ailments.

http://abcnews.go.com/Health/story?id=2959851&page=1



New risk factors discovered for Alzheimer's disease

A recent study in Journal of Neuroimaging suggests that cognitively normal adults exhibiting atrophy of their temporal lobe or damage to blood vessels in the brain are more likely to develop Alzheimer's disease. Older adults showing signs of both conditions were seven-times more likely to develop Alzheimer's than their peers.

http://www.blackwellpublishing.com/press/pressitem.asp?ref=1320



Scientists isolate chemical in curry that may help immune system clear plaques found in Alzheimer's

Researchers isolated bisdemethoxycurcumin, the active ingredient of curcuminoids -- a natural substance found in turmeric root -- that may help boost the immune system in clearing amyloid beta, a peptide that forms the plaques found in Alzheimer's disease.

http://www.eurekalert.org/pub_releases/2007-07/uoc--sic071307.php



'Human black box' found to boost long term memory in Alzheimer's sufferers

Scientists have found that Alzheimer's sufferers who were given a "human black box", have shown significant improvements in long-term memory.

http://www.dailyindia.com/show/128077.php/Human-black-box-found-to
-boost-long-term-memory-in-Alzheimers-sufferers



Scientists in Alzheimer's breakthrough

Japanese scientists have developed an oral vaccine for Alzheimer's disease that has proven effective and safe in mice, the research institute behind the project said today. The team is preparing to move to small-scale clinical trials in humans, possibly this year, said Takeshi Tabira, director of the National Institute for Longevity Sciences in Aichi, central Japan. "We hope the Phase I trials go well," Tabira said. "Animals are able to recover their functions after developing symptoms, but humans are less able to do so. It may be that this only works in the early stages of the disease, when symptoms are light."

http://www.ireland.com/newspaper/breaking/2007/0329/breaking12.htm



Protein that Directs Alzheimer's Development Found

The lack of CCR2 protien led to increased amyloid-beta deposits and earlier death in a mouse model of Alzheimer's disease. "Our results provide in vivo evidence that the brain's immune system plays a protective role in early Alzheimer's disease by mediating the clearance of amyloid-beta," says Joseph El Khoury, M.D., of the Massachusetts General Hospital Center for Immunology and Inflammatory Diseases.

http://www.genengnews.com/news/bnitem.aspx?name=14921056&source=genwire



Nursing home placement associated with accelerated cognitive decline in Alzheimer's disease

People with Alzheimer's disease experience an acceleration in the rate of cognitive decline after being placed in a nursing home according to a new study by Rush University Medical Center. The study, published in the June issue of the American Journal of Psychiatry, finds that prior experience in adult day care may lessen this association.

http://www.rush.edu/webapps/MEDREL/servlet/NewsRelease?ID=895



Blocking Immune Cell Action Increases Alzheimer's-associated Protein Deposits

The immune system's response against amyloid-beta, the protein that forms plaques in the brains of patients with Alzheimer's disease, appears to protect the brain from damage in early stages of the devastating neurological disorder. A report from Massachusetts General Hospital (MGH) researchers finds that lack of a protein required for recruitment of the brain's primary immune cell led to increased amyloid-beta deposits and earlier death in a mouse model of Alzheimer's disease.

http://www.sciencedaily.com/releases/2007/03/070327113731.htm



Yin and yang -- Balance could play key role in progression of Alzheimer's disease

Researchers at Rensselaer Polytechnic Institute are challenging current thinking on the causes and prevention of Alzheimer's disease, offering a new hypothesis that could be the key to preventing this form of dementia. The researchers have found that a specific imbalance between two peptides may be the cause of the fatal neurological disease that affects more than five million people in the United States.

http://news.rpi.edu/update.do?artcenterkey=2168&setappvar=page(1)



Blood inflammation plays role in Alzheimer's disease

People whose blood shows signs of inflammation are more likely to later develop Alzheimer's disease than people with no signs of inflammation, according to a study published in the May 29, 2007, issue of Neurology, the scientific journal of the American Academy of Neurology.

http://www.eurekalert.org/pub_releases/2007-05/aaon-bip052107.php



Alzheimer's Patients Are Dying Early Because Of Controversial Drugs

Results from a five-year project, funded by the Alzheimer’s Research Trust and presented at the charity’s conference in Edinburgh, found that the drugs were linked with a significant increase in long-term mortality - with patients dying on average six months earlier.

http://www.sciencedaily.com/releases/2007/03/070330230946.htm



Scientists identify new strategy for preventing acute and chronic brain disease

Scientists have found that reducing the level of the protein tau can prevent neurological deficits related to Alzheimer's disease.

http://www.gladstone.ucsf.edu/gladstone/site/publicaffairs/content.php?type=1&id=568



Estrogen Use Before 65 Linked to Reduced Risk of Alzheimer’s Disease

Women who use hormone therapy before the age of 65 could cut their risk of developing Alzheimer’s disease or dementia. This possibility is raised by research that will be presented at the American Academy of Neurology’s 59th Annual Meeting in Boston. The study found women who used any form of estrogen hormone therapy before the age of 65 were nearly 50 percent less likely to develop Alzheimer’s disease or dementia than women who did not use hormone therapy before age 65.

http://www.aan.com/press/index.cfm?fuseaction=release.view&release=471



Mayo Clinic Research Suggests Patterns of Brain Tissue Loss in Early Alzheimer's Disease May Predict Course of Disease

Magnetic resonance imaging (MRI) that shows patterns of brain tissue loss may help physicians predict which patients with amnestic mild cognitive impairment (early Alzheimer's disease) will develop full-blown Alzheimer's, according to findings of a Mayo Clinic study presented in Boston today at the annual meeting of the American Academy of Neurology.

http://www.mayoclinic.org/news2007-rst/4040.html



Study tests impact of omega-3 fatty acids on Alzheimer's disease

Nutritionists have long endorsed fish as part of a heart-healthy diet, and now some studies suggest that omega-3 fatty acids found in the oil of certain fish, algae and human breast milk may also benefit the brain by lowering the risk of Alzheimer’s disease. To test whether docosahexaenoic acid (DHA), an omega-3 fatty acid, can impact the progression of Alzheimer’s disease, researchers at the Suncoast Alzheimer’s and Gerontology Center at the University of South Florida, supported by the National Institute on Aging (NIA), part of the National Institutes of Health, will evaluate DHA in a clinical trial, the gold standard for medical research.

http://hscweb3.hsc.usf.edu/health/now/?p=101



Alzheimer's disease, Parkinson's disease

Alzheimer's disease, Parkinson's disease, type 2 diabetes, the human version of mad cow disease and other degenerative diseases are more closely related at the molecular level than many scientists realized, an international team of chemists and molecular biologists reported April 29 in the online version of the journal Nature.

http://www.newsroom.ucla.edu/page.asp?RelNum=7899



A possible mechanistic link between stress and the development of Alzheimer tangles

Subjecting mice to repeated emotional stress, the kind we experience in everyday life, may contribute to the accumulation of neurofibrillary tangles, one of the hallmarks of Alzheimer’s disease, report researchers at the Salk Institute for Biological Studies.

http://www.salk.edu/news/news_press_details_20070614.php



Newly discovered antibody may be body's natural defense against Alzheimer's

In an important advance in the battle against Alzheimer's disease, physician-scientists at NewYork-Presbyterian Hospital/Weill Cornell Medical Center have identified naturally occurring antibodies in human blood that may help to defend against this form of dementia as well as other neurodegenerative diseases.

http://www.nyp.org/news/hospital/antibody-target-oligomer.html



Natural protection to reduce spread of Alzheimer's disease

Podoly, 34, a native New Yorker, and his colleagues set out to design a blocker for the neurotoxic effects of the A? peptide, using the Butyrylcholinesterase (BChE) protein, which was cloned and engineered in their lab. BChE’s brain concentration increases with age, a fact overlooked so far, but which for Podoly and his colleagues seemed highly relevant to the progress of Alzheimer’s. The researchers set out in their laboratory to see if they could chemically improve and intensify BChE’s effect on the brain fibrils.

http://www.eurekalert.org/pub_releases/2007-06/thuo-hps061107.php



New Link Between Down Syndrome And Alzheimer's Disease

Scientists have shown that a protein involved in cholesterol metabolism may cause the accelerated onset of Alzheimer's Disease in individuals affected with Down Syndrome.

http://www.medicalnewstoday.com/medicalnews.php?newsid=69800



Secondhand Smoke Boosts Risk for Alzheimer's

Breathing in secondhand smoke could raise your risk for Alzheimer's disease and other forms of dementia, a new study finds.

http://www.cbc.ca/cp/HealthScout/070501/6050111AU.html



Breakdown of Myelin Implicated in Alzheimer’s, UCLA Research Shows

Wisdom comes with age (doesn't it?), but not without a process that takes place in the brain called myelination. Myelin is the fatty sheath that coats the axons of the nerves, allowing for efficient conduction of nerve impulses. It is key to the fast processing speeds that underlie our higher cognitive functioning, including, yes, wisdom.

http://www.newsroom.ucla.edu/page.asp?RelNum=7921


High doses of lithium-like drugs may impair neuronal function

New laboratory research suggests that lithium and other drugs that inhibit a particular enzyme, GSK-3 beta, should be used with caution in treating Alzheimer's disease because too high a dose can impair, rather than enhance, neuronal function. Lithium is currently in clinical trials for treating Alzheimer's. Pharmaceutical companies are interested in producing other GSK-3 beta inhibitors for the disease because these drugs are relatively easy to make and lithium has been shown to be safe in low doses in treating people with manic-depressive illness, said Dr. William D. Snider, professor of neurology, cell and molecular physiology at the University of North Carolina at Chapel Hill's School of Medicine. "People might think that if you make the inhibitor stronger and stronger, that would be better. Our in-vitro experiments show that you will have to be careful with how you use GSK-3 beta inhibitors, because if you use too much, it will interfere with and possibly kill neurons," said Snider, who also is director of UNC's Neuroscience Center

http://www.eurekalert.org/pub_releases/2006-12/uonc-hdo121906.php


Androgen Therapy May Slow Progress of Alzheimer's Disease

Experiments on mouse models of Alzheimer's disease (AD) suggest that treatment with male sex hormones might slow its progression. The findings, published in the December 20 issue of The Journal of Neuroscience, provide new insight into the relationship between testosterone loss and AD, which affects 4.5 million Americans.

Senior author Christian Pike, PhD, of the University of Southern California (USC), with colleagues at USC and the University of California, Irvine, sought to better understand the role hormones play in aging and disease. Recent studies had already established a link between testosterone loss in men and AD due to natural aging.

The research team established a correlation between low testosterone and elevated beta-amyloid (Aß), a protein that accumulates abnormally in AD patients. This finding, they say, suggests that testosterone depletion in aging men may be a risk factor for AD by promoting accumulation of Aß in the brain. Testosterone, the primary male sex hormone, is one in a group of related steroid hormones referred to as androgens. Recent studies suggest that androgens may lower Aß levels.

"This study raises the possibility that androgen replacement therapy might lower the risk for Alzheimer's, but this is far from proven," says Sam Gandy, MD, PhD, chair of the Alzheimer's Association's Medical and Scientific Advisory Council and director of the Farber Institute for Neurosciences at Thomas Jefferson University. "Because testosterone is rapidly converted to estrogen after entry into neurons, the new data are logical, and they dovetail well with historical data."

http://www.sfn.org/?pagename=news_121906a


Welsh scientists get breakthrough in fight against Alzheimer's

The team's research found that it is possible to decrease production of a small protein called *-amyloid (A*), which is believed to be the main cause of the disease. Deposits of A* build up in the brain, preventing it from functioning properly.

http://icwales.icnetwork.co.uk/0100news/0200wales/


Early diagnosis of Alzheimer is visible now

A new computerized technique can help in the early diagnosis of Alzheimer’s disease. With the help of this technique early signs of damaged cells caused by Alzheimer’s disease can be detected. This computer aided analysis is able to analyze the extent of damage areas of grey matter. The researchers say it could be treated most effectively in its initial stages. The University of California (Irvine) study appears in the journal, Radiology. Researcher Dr Min-Ying Su said “our methods may aid in earlier diagnosis of Alzheimer’s Disease, allowing earlier intervention to slow down disease progression”.

http://www.digitaldivide.net/articles/view.php?ArticleID=721


Alzheimer's treatment on horizon

An expensive new treatment may help remove errant proteins in the brain. An expensive new treatment may help remove errant proteins in the brain.

http://www.sptimes.com/2006/11/07/Floridian/Alzheimer_s_treatment.shtml


Drinking vegetable and fruit juice may prevent Alzheimer's

Drinking fruit and vegetable juice regularly may help to delay the onset of Alzheimer's disease, findings from a 10-year study suggest. A study of some 1,800 Japanese living in America aged 65 and above found that those who drank juice three or more times weekly had a much lower risk of developing the disease.

http://www.channelnewsasia.com/stories/health/view/239807/1/.html


Could Alzheimer’s be infectious?

One could predict that the accumulation of abnormal proteins in other neurodegenerative diseases - e.g. alpha-synuclein in Parkinson’s Disease and huntingtin in Huntington’s Disease, may also occur as a result of a prion-like seeding process. But for me, the most puzzling question of all is this: how would an Alzheimer’s infection be transmitted?

http://neurophilosophy.wordpress.com/2006/11/24/could-alzheimers-be-infectious/


Different forms of amyloid beta in Alzheimer's disease harm neurons in
different ways

Researchers at UC Irvine have shown that different forms of amyloid beta lead to neural damage in different ways, leading to an increasingly complex view of amyloid toxicity in the Alzheimer brain. The finding could modify the way therapeutic approaches for the treatment of Alzheimer’s disease are designed.

The researchers studied the effects of different forms of the amyloid beta peptide on human brain cells. Amyloid beta accumulation is one of two hallmarks of Alzheimer’s disease and is considered a major target for researchers looking into therapies for the treatment of the disease. After death, most amyloid beta found in the brains of Alzheimer’s patients is in fibrillar form – long, insoluble fibers bound together in deposits called senile plaques; however, there are also soluble forms of amyloid beta, or oligomers, that may decisively contribute to neural degeneration.

http://today.uci.edu/news/release_detail.asp?key=1484


Fish oil supplements seem to help Alzheimer's patients

This study randomly as-signed 204 people diagnosed with mild Alzheimer's to take fish oil supplements or a placebo daily. After six months, standardized tests of cognitive abilities showed similar declines in both groups. However, among only those with very mild cognitive dysfunction, people taking the supplements showed virtually no change, while the others declined.

http://www.twincities.com/mld/twincities/living/15943250.htm


28-Site Trial Studying Chinese Herb as Alzheimer’s Treatment

Researchers from Georgetown University Medical Center’s Memory Disorders Program are directing the first U.S. study to determine whether huperzine A, derived from the Chinese club moss plant Huperzia serrata, improves cognitive function in people with Alzheimer’s disease (AD). The study, which is recruiting participants at 28 sites across the country, is jointly funded by the National Institutes of Health and Neuro-Hitech Pharmaceuticals, Inc.

Huperzine A, a naturally occurring cholinesterase inhibitor, has been used in Chinese folk medicine for the treatment of fevers and inflammation. Although also commonly used in China to treat Alzheimer’s, there have been no controlled clinical trials assessing its toxicity and efficacy outside of China. Chinese studies have suggested that huperzine A is well tolerated and effective.

http://explore.georgetown.edu/news/?ID=15203


Huperzine A and Alzheimer

Huperzine A is a natural cholinesterase inhibitor derived from the Chinese herb Huperzia serrata. There is evidence that huperzine A may compare favorably in symptomatic efficacy to cholinesterase inhibitors currently in use. In addition, huperzine A has antioxidant and neuroprotective properties that suggest that it may be useful as a disease-modifying treatment for Alzheimer's disease (AD). The drug is currently available as a nutriceutical in tis country, and is being used by some U.S. clinicians to treat AD. However, there have been no controlled clinical trials outside China assessing its toxicity and efficacy

http://adcs.ucsd.edu/Huperzine_protocol.htm


Juices may reduce Alzheimer’s disease risk

A juice every other day could keep Alzheimer’s disease at bay, new research suggests. In a large epidemiological study, researchers found that people who drank three or more servings of fruit and vegetable juices per week had a 76 percent lower risk of developing Alzheimer’s disease than those who drank juice less than once per week. The study by Qi Dai, M.D., Ph.D., assistant professor of Medicine, and colleagues appears in the September issue of The American Journal of Medicine. The researchers followed a subset of subjects from a large cross-cultural study of dementia, called the Ni-Hon-Sea Project, which investigated Alzheimer’s disease and vascular dementia in older Japanese populations living in Japan, Hawaii and Seattle, Wash. For the current study, called the Kame Project, the researchers identified 1,836 dementia-free subjects in the Seattle population and collected information on their dietary consumption of fruit and vegetable juices. They then assessed cognitive function every two years for up to 10 years.

http://sitemason.vanderbilt.edu/newspub/crmQtG?id=28415


Microscopic Brain Damage Detected in Early Alzheimer's Disease

Researchers have developed a new computer-aided analysis technique to identify early cellular damage in Alzheimer's disease (AD). The study is featured in the October issue of Radiology. "With increasing longevity among the population, the incidence of AD is expected to rise rapidly, creating a great burden not only for patients and their families, but also for society," said Min-Ying Su, Ph.D., author and associate professor in the Department of Radiological Sciences & the Tu and Yuen Center for Functional Onco-Imaging at the University of California at Irvine. "Our methods may enable earlier diagnosis of AD, allowing earlier intervention to slow down disease progression," she added. As AD progresses, cell membranes in the brain may be damaged, allowing water molecules to move throughout the brain more freely. This phenomenon can disrupt neural processes and cause neuron cells to die, leading to brain atrophy. This process of cellular damage causes an increase in the "apparent diffusion coefficient," or ADC, which is a measurement used to study the distribution of water in the brain.

http://www2.rsna.org/pr/target.cfm?ID=288


Alzheimer research forum

The Alzheimer Research Forum, founded in 1996, is the web's most dynamic scientific community dedicated to understanding Alzheimer's disease and related disorders. Access to the web site is free to all. Our editorial priorities are as diverse as the needs of the research community. The web site reports on the latest scientific findings, from basic research to clinical trials; creates and maintains public databases of essential research data and reagents, and produces discussion forums to promote debate, speed the dissemination of new ideas, and break down barriers across the numerous disciplines that can contribute to the global effort to cure Alzheimer's disease.

http://www.alzforum.org/


Researchers Identify Brain Protein that Halts Progression of Alzheimer's

Researchers have identified a protein in the brain that halts the progression of Alzheimer's disease in human brain tissue. The protein, known as "transthyretin," protects brain cells from gradual deterioration by blocking another toxic protein that contributes to the disease process.

http://www.niehs.nih.gov/oc/news/brainpr.htm


UCI researchers identify first compound to block progression of Alzheimer’s disease

Researchers at UC Irvine have found that a new compound not only relieves the cognitive symptoms of Alzheimer’s disease, but also reduces the two types of brain lesions that are hallmarks of this devastating disease, thereby blocking its progression.

http://today.uci.edu/news/release_detail.asp?key=1447


Proprietary Therapeutics for Alzheimer's Disease

IIBR has launched a major R&D program focused on the design, development and testing of novel drug compounds for the treatment of central nervous system disorders such as Alzheimer’s disease (AD). The program is based on manipulation of specific neurotransmitter systems believed to be involved in a range of neuropsychiatric diseases.

http://www.iibr.gov.il/medicinal001.asp


Anti-Inflammatory Function of Alzheimer’s Disease Drugs Revealed by HU Researchers

The mechanism in anti-Alzheimer’s disease drugs that inhibits the production of a destructive, inflammation-causing protein in the brain has been revealed by researchers at the Hebrew university of Jerusalem.

http://www.hunews.huji.ac.il/articles.asp?cat=6&artID=501


Gladstone scientists prove neurons produce Alzheimer's-linked apolipoprotein E

A question long debated among Alzheimer's disease researchers has been definitively answered by scientists at the Gladstone Institute of Neurological Disease in San Francisco. Using a unique mouse model, Gladstone Investigator Yadong Huang, MD, PhD, and his team have proven that, under certain conditions, neurons produce Alzheimer's-linked apolipoprotein E. Also known as apoE, this cholesterol-carrying protein has three common forms, one of which, apoE4, is the major known genetic risk factor for Alzheimer's disease, according to studies published around the world in recent years. Until now, most researchers have believed that apoE is synthesized in the brain solely in such cells as astrocytes, microglia, and ependymal layer cells. Controversial for the last decade has been the question of whether or not neurons, which make thought and memory possible by transmitting electrical signals, can produce apoE.

http://www.eurekalert.org/pub_releases/2006-05/gi-gsp051006.php


CoQ10 may protect against Alzheimer’s

Increasing intake of coenzyme Q10 may ward off the threat of Alzheimer’s disease, if the results of an animal study can be applied to humans. The body's manufacture of CoQ10 begins to drop after the age of about 20, leading to its investigation in age-related disease. It has been shown to help prevent Parkinson's and is also thought to prevent skin ageing

http://www.nutraingredients.com/news/ng.asp?
n=67263-coq-alzheimer-s-antioxidant


Effects of Coenzyme Q10 in Early Parkinson Disease

Coenzyme Q10 was safe and well tolerated at dosages of up to 1200 mg/d. Less disability developed in subjects assigned to coenzyme Q10 than in those assigned to placebo, and the benefit was greatest in subjects receiving the highest dosage. Coenzyme Q10 appears to slow the progressive deterioration of function in PD, but these results need to be confirmed in a larger study.

http://archneur.ama-assn.org/cgi/content/abstract/59/10/1541


Rol van insuline bij Alzheimer

Brown Medical School (US) brengt insuline in het middelpunt van de belangstelling. Men vond abnormaal lage niveaus van insuline en insuline groeifactoren in delen van de hersenen die het meest waren aangetast door Alzheimer, en men vond dat deze lage niveaus bijdroegen tot “brain rotting”. Eerder onderzoek toonde aan dat insuline helpt bij het reguleren van amyloid en de vorming van destructieve vormen van tau helpt te voorkomen. Studies vonden tevens dat mensen met type 2 diabetes, waarbij de cellen ongevoelig worden voor insuline, een groter risico lopen op het ontwikkelen van Alzheimer.

http://www.hulporganisaties.be/Pages/details.asp?lng=NL&Id=1833


A new species of amyloid peptide

Scientists have identified a new, longer species of amyloid ß-peptide that has the potential to be a new target for the treatment of Alzheimer's disease.

The research appears as the "Paper of the Week" in the December 3 issue of the Journal of Biological Chemistry, an American Society for Biochemistry and Molecular Biology journal.

One of the characteristic features of Alzheimer's disease is the deposition of amyloid ß-peptides in the brain. These amyloid ß-peptides are derived from a large amyloid precursor protein through a series of cleavage events. Under normal conditions, cleavage first by a-secretase and then by ?-secretase results in a soluble ectodomain, a short peptide called p3, and an intracellular C-terminal domain, none of which are amyloidogenic. Alternatively, amyloid precursor protein can be processed by the enzymes ß-secretase and ?-secretase to produce a soluble ectodomain along with the full-length amyloidogenic amyloid ß-peptide and the intracellular C-terminal domain.

Although amyloid precursor protein is found in many cells, its normal biological function is not well understood. "It has been suggested that amyloid precursor protein may function as a receptor or growth factor precursor," notes Dr. Xuemin Xu of The University of Tennessee. "Recent studies also suggest that the intracellular C-terminal domain of the amyloid precursor protein may function as a transcription factor."

While the exact pathogenic role of amyloid ß-peptide in Alzheimer's disease has not yet been definitely established, accumulating evidence supports the hypothesis that amyloid ß-peptide production and deposition in the brain could be a causative event in Alzheimer's disease. Dr. Xu explains that the literature indicates amyloid ß-peptide itself could be toxic to synapses and the accumulation of amyloid ß-peptide could initiate a series of events contributing to cell death, including activation of cell death programs, oxidation of lipids and disruption of cell membranes, an inflammatory response, and possibly neurofibrillary tangle formation, which is a close correlate of neuron loss. Therefore, the problem of production, accumulation, and clearance of amyloid ß-peptide in the brain emerges as one of the possible rational approaches for the treatment of Alzheimer's disease.

Generally, amyloid ß-peptides are around 39-43 amino acid long. Studies have shown that the longer amyloid ß-peptides are more amyloidogenic and more pathogenic than the shorter ones. Now, Dr. Xu and his colleagues have discovered a new species of amyloid ß-peptide that is 46 amino acids long, called Aß46. This Aß46 peptide is produced by ?-secretase at a novel cleavage site, the ?-site. This site also happens to be the site of a mutation found in early-onset familial Alzheimer's disease called the APP717 or London mutation.

"Another well characterized Alzheimer's disease-linked amyloid precursor protein mutation, the Swedish mutation, also occurs at a major cleavage site, the ß-cleavage site at the N-terminus of amyloid ß-peptide," adds Dr. Xu. "Studies have shown that Swedish mutation at the ß-cleavage site makes the amyloid precursor protein more susceptible to ß-secretase activity. The finding that ?-cleavage site is the APP717 mutation site suggests that the APP717 mutation may cause enhanced production of the longer amyloid ß-peptide, Aß42, by influencing the ?-cleavage. Therefore, this finding may open a new avenue for studying the mechanism by which APP717 mutations cause enhanced production of the longer amyloid ß-peptide."

Dr. Xu and his colleagues also discovered that ?-secretase cleavage at the new ?-site is specifically inhibited by compounds known as transition state analogs, but is less affected by compounds known as non-transition state inhibitors. Specifically, some of these inhibitors, which were previously known to inhibit the formation of secreted amyloid ß-peptides, were found to cause an intracellular accumulation of an even longer amyloid ß-peptide species, Aß46. "These novel findings provide information important for the strategy of prevention and treatment of Alzheimer's disease, aimed at the design of ?-secretase inhibitors," concludes Dr. Xu. "Since amyloid ß-peptide is produced by the sequential actions of ß- and ?-secretases, inhibition of these secretases to reduce the production of amyloid ß-peptide is believed to be one of the more promising avenues of treatment of the disease. To date, more than one dozen ?-secretase inhibitors have been developed or identified."


Walnuts and Alzheimer

Many think melatonin is something you can take to fall asleep after long airplane flights, but scientists are studying how this powerful antioxidant actually fights diseases like cancer, may impact diseases associated with aging and likely will allow people to live healthier lives. Research at The University of Texas Health Science Center in San Antonio has proven walnuts are a natural source of melatonin.

According to Russel J. Reiter, Ph.D., Professor of Neuroendocrinology at The
University of Texas Health Science Center at San Antonio, 'The ingredients in walnuts would be expected to reduce the incidence of cancer, delay or make less severe neurodegenerative diseases of aging, including Parkinsonism, Alzheimer's disease and reduce the severity of cardiovascular disease.' Published in the September issue of Nutrition: The International Journal of Applied and Basic Nutritional Sciences, the study is titled 'Melatonin in walnuts: Influence on levels of melatonin and total antioxidant
capacity of blood.'

Dr. Reiter's study found walnuts are a potent source of melatonin, which is easily absorbed in the body. 'When walnuts are consumed, blood levels of melatonin increase threefold,' notes Reiter. Studies have shown walnuts reduce the risk of heart disease due to their combination of healthy nutrients, including omega-3 fatty acids and antioxidants.
Reiter believes it is the synergy among the ingredients in walnuts -- the combination of nutrients plus the melatonin that makes them so beneficial. 'Melatonin and omega-3s, both of which are in walnuts, starve cancers because they prevent the growth of cancer cells. When you take melatonin as a tablet, you are exclusively getting melatonin. I think the
value of the walnut is the composite of what it contains.'


Study Reveals Possible Location of Alzheimer's Genes

Researchers at Columbia University Medical Center have found two locations in the human genome that may harbor genes which increase the risk of Alzheimer's disease. If confirmed, they will be the first genes linked to the disease since ApoE4 was discovered in 1993. The findings are published in the November issue of Molecular Psychiatry, a journal of the Nature Publishing Group.

"We feel confident that we may be closing in on new Alzheimer's genes," says the study's senior author, Richard Mayeux, co-director of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at CUMC. "This is a major collection of families, and family studies really give you more confidence that the region you're looking at is significant."

Researchers think that Alzheimer's is caused by the interaction of several different genes, but so far only one gene, ApoE4, has been linked conclusively to the disease. Finding the other genes will be a huge step toward understanding how Alzheimer's begins and how it can be treated. It will also allow clinicians to predict who will develop Alzheimer's later in life and who will benefit from drugs that prevent the disease.

The new study found strong evidence for new Alzheimer's genes on chromosomes 18 and 10. The region on 18 had never been strongly linked to the disease before, but the link to chromosome 10 confirms previous findings by other Alzheimer's researchers.

The evidence for both locations is relatively strong because the researchers used a large collection of 96 families with Alzheimer's disease. A total of 490 parents, children and siblings were studied.

The researchers do not yet know which gene in the chromosome 18 region is responsible, but since the region is small, there are only a few possibilities. The region on chromosome 10 had been linked to Alzheimer's before, but only in studies of Caucasian families. The current study found the link in Caribbean Hispanic families, most of whom live in the Dominican Republic.

"To find the same location in a different ethnic group strongly suggests that there's a gene for Alzheimer's in that region," Mayeux says. "Human diseases should cause disease in every ethnic group."

Source: Richard Mayeux, Columbia University New York USA


Possible New Treatment Strategy for Alzheimer's Disease, Say Researchers

A new study in mice identifies one of the missing steps in how Alzheimer's develops and suggests a possible new treatment strategy, according to researchers at Columbia University Medical Center and Weill Cornell Medical College and their colleagues. The results of the study are to be published in the April 16 issue of Science.

The researchers, led by Shi Du Yan, M.D., associate professor of clinical pathology and member of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain; Joyce W. Lustbader, Ph.D., senior research scientist in obstetrics and gynecology; and Hao Wu, Ph.D., at Weill Cornell, created a crystal form of two molecular components of the disease.

"The crystal complex is the first demonstration that beta-amyloid peptide binds to a protein called ABAD and accumulates inside the mitochondria in brain cells," Lustbader said. Many researchers believe that Alzheimer's occurs when beta-amyloid clusters in and ultimately kills brain cells by causing the production of destructive free radicals in the mitochondria.

"Our findings suggest that one way to treat Alzheimer's would be to develop a drug that prevents the beta-amyloid peptides from binding with ABAD, which might prevent the cascade of damage that Alzheimer's typically leads to," Yan said.

Source: Columbia University New York USA


CU Researchers Design Tool to Detect Alzheimer's Early

Doctors have long known that smell is one of the first senses to fail as Alzheimer's begins its slow and incurable progression. Tracking the process whereby a person loses their ability to smell could play a pivotal role in early detection and treatment of Alzheimer's. And now researchers at Columbia have developed a tool that will aid early detection.

The system that governs our sense of smell is centered in the same area of the brain that is first attacked, then damaged, during the original stages of Alzheimer's. But for researchers such as Davangere Devanand, professor of psychiatry and neurology at Columbia University Medical Center, the perplexing issue was, exactly which smells people lose the ability to recognize. Could memory loss be detected soon enough to allow for early treatment, and once isolated, what might findings about smell loss suggest for developing detection and treatment methods for Alzheimer's?

There are 4.5 million Americans suffering from Alzheimer's, with an estimated annual medical tab of $100 billion in related treatment and health care costs. This fact was not lost on Devanand, who clearly saw the value in examining the link between diminished smell and Alzheimer's.

To discover possible connections, Deavand and his team assembled a test group of 150 people, from 43 to 85 years old, and with varied degrees of memory loss. To establish a baseline, this group was initially tested then re-tested every six months in order to measure overall ability to identify 10 separate smells: lemon, leather, clove, lilac, menthol, pineapple, natural gas, soap, strawberry and lavender. The results were compared to a control group of 63 healthy volunteer with no memory impairment. Volunteers were given scented cards and asked to identify a series of smells. The results, gathered over nine years, indicated that volunteers who preformed poorly at identifying the smells over time went on to develop Alzheimer's. None of the non-afflicted subjects developed the disease.

Devanand says, "Early diagnosis of Alzheimer's disease is critical for patients and their families to receive the most beneficial treatment and medications." He added that tests such as these may very soon go a long way toward helping detect Alzheimer's far sooner than is currently possible. He recently presented his findings at a meeting of the American College of Neuropsychopharmacology.

The trial conducted by Devanand and his team also lays important groundwork for future advances. For now, the medical community has another valuable early indicator of the progression of the disease. But in future, medical investigators will be able to build on the work of Devanand and his researchers to perhaps find a cure for Alzheimer's.

Source: Columbia University New York USA, David Poratta


New Dye Could Offer Early Test For Alzheimer's


Massachusetts Institute of Technology (MIT) scientists have developed a new dye that could offer noninvasive early diagnosis of Alzheimer's disease, a discovery that could aid in monitoring the progression of the disease and in studying the efficacy of new treatments to stop it. The work is published in the August 26 issue of Angewandte Chemie.

Today, doctors can only make a definitive diagnosis of Alzheimer's—currently the fourth-leading cause of death in the United States—through a postmortem autopsy of the brain. "Before you can cure Alzheimer's, you have to be able to diagnose it and monitor its progress very precisely," said Timothy Swager, leader of the work and a professor in MIT's Department of Chemistry. "Otherwise it's hard to know whether a new treatment is working or not."

To that end, Swager and postdoctoral associate Evgueni Nesterov, also from the MIT Department of Chemistry, worked with researchers at Massachusetts General Hospital and the University of Pittsburgh to develop a contrast agent that would first bind to the protein deposits, or plaques, in the brain that cause Alzheimer's, and then fluoresce when exposed to radiation in the near-infrared range. The new dye could allow direct imaging of Alzheimer's plaques through a patient's skull.

Some of the first noninvasive techniques for diagnosing Alzheimer's involved agents labeled with radioactive elements that could enter the brain and target disease plaque for imaging with positron emission tomography (PET). However, these methods were expensive and limited by the short working lifetime of the labeled agents.

Swager and colleagues developed the new dye, called NIAD-4, through a targeted design process based on a set of specific requirements, including the ability to enter the brain rapidly upon injection, bind to amyloid plaques, absorb and fluoresce radiation in the right spectral range, and provide sharp contrast between the plaques and the surrounding tissue. The compound provided clear visual images of amyloid brain plaques in living mice with specially prepared cranial windows.

To make the technique truly noninvasive, scientists must further refine the dye so it fluoresces at a slightly longer wavelength, closer to the infrared region. Light in the near-IR range can penetrate living tissue well enough to make brain structures visible. Swager likens the effect to the translucence produced when one holds a red laser pointer against the side of a finger.

Swager says fluorescing dyes like NIAD-4 could be ready for clinical trials in the near future.

Source: Massachusetts Institute of Technology


Study Links Alzheimer's Disease to Abnormal Cell Division

Overview A new study in mice suggests that Alzheimer's disease (AD) may be triggered when adult neurons try to divide. The finding helps researchers understand what goes wrong in the disease and may lead to new ways of treating it.

A new study in mice suggests that Alzheimer's disease (AD) may be triggered when adult neurons try to divide. The finding helps researchers understand what goes wrong in the disease and may lead to new ways of treating it. The study was funded in part by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, and appears in the January 18, 2006 issue of The Journal of Neuroscience.[1]

For unknown reasons, nerve cells (neurons) affected by AD and many other neurodegenerative diseases often start to divide before they die. The new study shows that, in animal models of AD, this abnormal cell division starts long before amyloid plaques or other markers of the disease appear. Cell division occurs through a process called the cell cycle. “If you could stop cell cycling, you might be able to stop neurons from dying prematurely. This could be a fresh approach to therapy for Alzheimer's and other diseases, including stroke, amyotrophic lateral sclerosis [also known as Lou Gehrig's disease], and HIV dementia,” says Karl Herrup, Ph.D., of Case Western Reserve University in Cleveland, who led the study.

The researchers compared the brains of three different mouse models of AD to brains from normal mice, looking specifically for markers of cell cycling. They found that, in the AD mouse models, cell cycle-related proteins appeared in neurons 6 months before the first amyloid plaques or disease-related immune reactions developed in the brain. Many of the neurons also had increased numbers of chromosomes, which is typical of cells that have begun to divide. These changes were not seen in normal mice. The regions of the brain most affected by the neuronal cell cycling were the cortex and the hippocampus – the same regions most affected in AD. The cortex is important for thought and reasoning, while the hippocampus plays a key role in learning and memory. Some parts of the brainstem also showed evidence of cell cycling.

While the cell cycling appeared to be necessary for neurons to die, it was not an immediate cause of cell death in the mouse models of AD. Instead, the affected neurons appeared to live for many months in a near-functional state, with the mice showing only mild behavioral changes during that time. This suggests that another type of cellular problem, still unidentified, must damage the neurons in order for them to die.

The findings shed new light on the theory that the accumulation of amyloid beta in the brain causes the neuron death in AD. Because the abnormal cell cycling begins months before the formation of amyloid plaques, it is unlikely that the plaques themselves trigger the disease process. However, tiny clumps made up of several amyloid beta molecules (called micro-molecular aggregates) form before the plaques and may trigger the disease. Since the three mouse models tested in this study all had mutations in the gene that codes for amyloid precursor protein, the similarity between affected brain regions in these mice and in people with AD also supports the amyloid hypothesis.

While previous studies have linked AD to abnormal cell cycling, this is the first study to examine the link using standard mouse models of AD. The results indicate that the mice, which do not develop neurofibrillary tangles or the severe behavioral symptoms of AD, are accurate models of the early cellular processes that lead to the disease. "The cell cycle markers mimic the human situation rather well," says Dr. Herrup. "This opens a range of new experimental possibilities using the cell cycle events as indicators of neuronal distress."

Dr. Herrup and his colleagues are now trying to determine if feeding the mouse models the drug ibuprofen can stop abnormal cell cycling in neurons and halt neurodegeneration. Ibuprofen is an anti-inflammatory drug that reduces production of amyloid beta, and some studies have suggested that it may reduce the risk of AD. The researchers are also planning additional studies to identify why neurons start to divide when they are diseased and why entering the cell cycle appears to trigger cell death.

The NINDS is a component of the National Institutes of Health (NIH) within the Department of Health and Human Services and is the nation’s primary supporter of biomedical research on the brain and nervous system. The NIH is comprised of 27 Institutes and Centers. It is the primary Federal agency for conducting and supporting basic, clinical, and translational medical research, and investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

The work was conducted at Case Western Reserve University's Alzheimer's Disease Center, which is directed by Dr. Herrup and supported by the National Institute on Aging, also part of the NIH.

[1]YangY, Varvel NH, Lamb BT, Herrup K. Ectopic cell cycle events link human Alzheimer’s disease and APP transgenic mouse models. The Journal of Neuroscience, January 18, 2005, Vol. 26, No. 3, pp. 775-784.


Causes of Alzheimer

Scientists have identified several factors that appear to play a role in the development of Alzheimer’s disease (AD) but have not yet reached any firm conclusions as to exactly what causes the disease. When scientists examine the brains of AD patients under the microscope, they see two types of abnormalities: neuritic plaques and neurofibrillary tangles. Neuritic plaques are spherical structures containing protein, nerve cell fragments, and other cells. Neurofibrillary tangles, as the name suggests, are tangled fibers found inside nerve cells, or neurons. Many scientists think that the plaques and tangles interfere with communication among neurons in the brain, thereby disrupting mental activity. These structures also seem to participate in processes that kill neurons.

http://www.ahaf.org/SubIndex/AD_PDF_FactSheets


Alzheimer's Disease Education & Referral Center

AD is named after Dr. Alois Alzheimer, a German doctor. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. He found abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary tangles). Today, these plaques and tangles in the brain are considered signs of AD.

Scientists also have found other brain changes in people with AD. Nerve cells die in areas of the brain that are vital to memory and other mental abilities, and connections between nerve cells are disrupted. There also are lower levels of some of the chemicals in the brain that carry messages back and forth between nerve cells. AD may impair thinking and memory by disrupting these messages.

http://www.alzheimers.org/


New structure of Alzheimer’s drug predicted by e-Materials project

The UCL-led e-Materials project has achieved one of the holy grails of the pharmaceutical industry – the computational prediction of a previously unidentified crystal structure, or polymorph, of a drug molecule.Researchers working on the project have successfully predicted a new polymorph of the Alzheimer’s drug, Piracetam. The action of a drug is dependent not only on its chemical composition, but also on the way in which the drug molecules arrange themselves. For example, crystal structure can affect the drug’s solubility and hence its rate of absorption into the bloodstream. An unexpected polymorph could alter the drug’s therapeutic properties if it inadvertently contaminated the standard formulation.

http://www.ucl.ac.uk/news/news-articles/06010902


Mediterranean Diet Lowers Alzheimer’s Risk in American Cohort

Americans who ate a Mediterranean diet—lots of fruits, vegetables, legumes, cereals, some fish and alcohol, and little dairy and meat—had a reduced risk for Alzheimer’s disease as they aged. These findings are published in the April issue of Annals of Neurology, a journal published by John Wiley & Sons.

http://www3.interscience.wiley.com/cgi-bin/jabout/
76507645/News.html?CRETRY=1&SRETRY=0


PLD1 protein is implicated in Alzheimer’s brain damage

Most current Alzheimer’s drugs target molecules responsible for memory formation. But while helpful at slowing and even reversing memory loss, this approach doesn’t address the root of the problem: plaques that build amid brain cells, causing them to weaken and die. In back-to-back papers published online in Proceedings of the National Academy of Sciences, Dongming Cai and other Rockefeller scientists, in the research group led by Paul Greengard, now say that a protein called PLD1 may be a target for new drugs that better treat — or even prevent — Alzheimer’s.

http://newswire.rockefeller.edu/?page=engine&id=471


Elevation of serum copper levels in Alzheimer's disease

Copper may play a role in neurodegenerative processes in AD, and serum copper measurement may prove to be a peripheral diagnostic marker for AD.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=
Retrieve&db=PubMed&dopt=Abstract&list_uids=12391342


Ab initio model studies of copper binding to peptides containing a His-His sequence: relevance to the beta-amyloid peptide of Alzheimer's disease.

The Cu2+ concentrations in cores of senile plaques are significantly elevated in AD patients. Experimental results indicate that Abeta1-42 in particular has a very high affinity for Cu2+, and that His13 and His14 are the two most firmly established ligands in the coordination sphere of the copper ion.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=
pubmed&dopt=Abstract&list_uids=16267663&query
_hl=2&itool=pubmed_DocSum


Kupfer – eine neue Chance zur Behandlung von Alzheimer?

Aufgrund der viel versprechenden Ergebnisse der biochemischen Forschung und der tierexperimentellen Beobachtungen hat man sich in der Klinik für Psychiatrie und Psychotherapie des Universitätsklinikums des Saarlandes (Direktor: Prof. Dr. Peter Falkai) dazu entschlossen, erstmals eine klinische Studie für Alzheimer-Patienten durchzuführen. Die Studie wird von Prof. Dr. Thomas Bayer, wissenschaftlicher Leiter, und Privatdozent Dr. Frank-Gerald Pajonk, Leiter der Klinischen Prüfung und Geschäftsführender Oberarzt der Klinik, betreut. Mit dieser Studie wollen die Mediziner klären, ob durch die Einnahme von Kupfer als Nahrungsergänzungsmittel bei Patienten mit beginnender Alzheimer-Erkrankung das Fortschreiten der Demenz aufgehalten werden kann. „Die Vermutung liegt bereits jetzt sehr nahe, dass dies der Fall ist, doch den endgültigen Beweis kann nur eine abgeschlossene klinische Studie erbringen“, erläutert Privatdozent Dr. Frank-Gerald Pajonk.

http://www.uniklinikum-saarland.de/de/aktuelles/
pressemitteilungen/2006/02/1138954962


How does oxidation work in neurodegenerative disease?

The nervous system, including the brain, spinal cord, and peripheral nerves, is rich in both unsaturated fats (which are prone to oxidation) and iron (Halliwell 1992). The high lipid content of nervous tissue, coupled with its high metabolic (aerobic) activity, makes it particularly susceptible to oxidant damage (Dawson and Dawson 1996). The high level of brain iron may be essential, particularly during development, but its presence also means that injury to brain cells may release iron ions that can lead to oxidative stress via the iron-catalyzed formation of reactive oxygen species (Gerlach et al. 1994).

http://www.astaxanthin.org/neurodisease.htm


Loss of Body Mass Linked to Development of
Alzheimer’s Disease, Study Finds

Loss of body mass over time appears to be strongly linked to older adults’ risk of developing Alzheimer’s disease (AD), and the greater the loss the greater the chance of a person developing the disease, new research has found. The findings are the first to associate decline in body mass index (BMI) with the eventual onset of AD. The researchers suggest that the loss of body mass reflects disease processes and that change in BMI might be a clinical predictor of the development of AD.

The research, reported in the September 27, 2005, issue of Neurology, was conducted by Aron S. Buchman, M.D., David A. Bennett, M.D., and colleagues at Rush University Medical Center in Chicago, IL, as part of the Religious Orders Study. The Religious Orders Study is a comprehensive, long-term look at aging and AD among Catholic nuns, priests, and brothers nationwide that has been funded by the National Institute on Aging (NIA), a component of the National Institutes of Health, U.S. Department of Health and Human Services, since 1993. Rush University Medical Center is one of more than 30 Alzheimer’s Disease Centers supported by the NIA.

“People with Alzheimer’s disease are known to lose weight and body mass after they have the disease,” says Dallas W. Anderson, Ph.D., program director for population studies in the Dementias of Aging Branch of NIA’s Neuroscience and Neuropsychology of Aging Program. “This study is significant in that it looks at body mass changes in the years preceding dementia and cognitive decline. Other studies have looked at BMI at only one point in time or studied body mass loss in people who already have AD.”

www.alzheimers.org/nianews/nianews75.htm


Insulin Insults May Spur Alzheimer's Disease

Science 4 July 2003:
Vol. 301. no. 5629, pp. 40 - 41
DOI: 10.1126/science.301.5629.40

Evidence has accumulated that pancreatic control of the hormone insulin may play an important role in the genesis of Alzheimer's disease. Excess insulin, some suggest, may help litter the brain with senile plaques.


Association between features of the insulin resistance syndrome and alzheimer's disease independently of apolipoprotein e4 phenotype: cross sectional population based study

Johanna Kuusisto, lecturer in medicine,a Keijo Koivisto, consultant physician,b Leena Mykkänen, consultant physician,a Eeva-Liisa Helkala, psychologist,b Matti Vanhanen, psychologist,b Tuomo Hänninen, psychologist,b Kari Kervinen, consultant physician,c Y Antero Kesäniemi, professor,c Paavo J Riekkinen, professor,b Markku Laakso, professor a
a Department of Medicine, Kuopio University Hospital, PO Box 1777, FIN-70211 Kuopio, Finland, b Department of Neurology, Kuopio University Hospital, c Department of Internal Medicine, Oulu University Hospital and Biocenter Oulu, University of Oulu, Oulu, Finland

Features of the insulin resistance syndrome are associated with Alzheimer's disease independently of apolipoprotein E4 phenotype.

In conclusion, features of the insulin resistance syndrome are associated with Alzheimer's disease, independently of the apolipoprotein E4 phenotype. Alzheimer's disease may resemble coronary heart disease, in which several factors contribute to the risk for the disease. Even more importantly, as the insulin resistance syndrome is at least in part preventable by modification of life style, Alzheimer's disease might also be preventable, at least in some cases, thus opening new areas for researchers.


Discovery that insulin is produced in the brain raises possibility of Type 3 diabetes

Researchers at Rhode Island Hospital and Brown Medical School have discovered that insulin and its related proteins are produced in the brain, and that reduced levels of both are linked to Alzheimer's disease.

http://www.medicalnewstoday.com/medicalnews.php?newsid=20838


Journal of Alzheimer's Disease

The Journal of Alzheimer’s Disease is an international multidisciplinary journal with a mission to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer’s disease.

http://www.j-alz.com/


Intake of dietary copper helps Alzheimer's patients

As one of the services for patients with Alzheimer's disease, the Department of Psychiatry at the Saarland University Medical Center offers participation in a clinical phase II trial. This clinical trial aims to elucidate a potential beneficial effect of copper orotate (an organic copper salt), which is given together with a standard cholinesterase inhibitor. A diagnosis of mild to moderate dementia of the Alzheimer type is a prerequisite. Besides clinical investigations, laboratory investigations of blood and cerebrospinal fluid, and magnet resonance imaging of the brain will be carried out. The study is being conducted by Professor Dr. Thomas Bayer, the Head of the Division of Neurobiology, and Dr. Frank Pajonk, a Psychiatrist, at the Department of Psychiatry, Saarland University Medical Center.

In the present study, the teams led by Bayer and Multhaup have found that low copper level in blood correlates with advanced memory deficits, as tested by the well established ADAS-cog neuropsychological test battery. Patients with higher blood copper levels make fewer mistakes in this memory test. This result supports the notion of a mild copper deficiency in AD patients. An increased uptake of dietary copper may therefore be therapeutically relevant.

Priv. Doz. Dr. med. Frank-Gerald B. Pajonk
Geschäftsführender Oberarzt der Klinik für Psychiatrie und Psychotherapie,
Universitätsklinikum des Saarlandes in Homburg/Saar

Tel. (06841) 16-24205
Fax (06841) 16-24270
E-Mail: frank.pajonk@uniklinikum-saarland.de


Age-related memory improvement linked with consumption of apple products

New study finds consuming apple juice associated with brain health

"An apple a day" now has new meaning for those who want to maintain mental dexterity as they age. New research from the University of Massachusetts Lowell suggests that consuming apple juice may protect against cell damage that contributes to age-related memory loss, even in test animals that were not prone to developing Alzheimer's disease and other dementias.

"This new study suggests that eating and drinking apples and apple juice, in conjunction with a balanced diet, can protect the brain from the effects of oxidative stress – and that we should eat such antioxidant-rich foods," notes lead researcher Thomas B. Shea, Ph.D., director of the University of Massachusetts Lowell's Center for Cellular Neurobiology and Neurodegeneration Research, whose study was just published in the latest issue of the Journal of Alzheimer's Disease. Although more research is needed, Shea is excited about these brain health findings, which are encouraging for all individuals who are interested in staying mentally sharp as they age.

Using a well-established animal protocol, Shea and his research colleagues assessed whether consumption of apple juice was protective against oxidative brain damage in aging mice, damage that can lead to memory loss. "These newer findings show that there is something in apples and apple juice that protects brain cells in normal aging, much like the protection we previously saw against Alzheimer-like symptoms," says Shea.

The researchers evaluated adult and aged mice using a standard diet, a nutrient-deficient diet, and a nutrient-deficient diet supplemented with apple juice concentrate in drinking water. Although the adult mice tested were not affected negatively by the deficient diets, the aged mice were, which is consistent with normal aging due to oxidative neurodegeneration. The effect on cognition among the aged mice was measured through well-established maze tests, followed by an examination of brain tissue. However, the aged mice who consumed the diets supplemented with apple juice performed significantly better on the maze tests and all had less oxidative brain damage than those on the standard diet.

Supplementation by apple juice fully protected the aged mice from the oxidative stress caused by the nutrient-deficient diet. In addition, stronger mental acuity resulted when the aged mice consumed the human equivalent of 2-3 cups of apple juice or approximately 2-4 apples per day. "We believe that this effect is due to the apple's naturally high level of antioxidants," states Shea. Previous research with his colleagues also determined that it is not the sugar and energy content of the apple juice, but the antioxidant attributes of apple juice that are responsible for the positive effects.


Fruit, vegetable juices may stall Alzheimer's disease

Certain polyphenols abundant in fruit and vegetable juices may play an important role in delaying the onset of Alzheimer’s disease, reports Dominique Patton. Amy Borenstein from the University of South Florida said yesterday that her team had found a 75 per cent reduced risk of the disease among elderly people who drank fruit or vegetable juices at least three times per week compared with those who drank these juices less than once a week. There was no apparent dementia-related benefit from dietary or supplemental vitamin E, C or beta-carotene intake, she added.

The research was presented at the US-based Alzheimer\'s Association’s first conference on prevention of dementia, running in Washington this week (abstract 05-A-103-ALZ-PC). There are nearly 18 million people with dementia in the world and the most common cause of this dementia is Alzheimer’s disease. By 2025 this figure will rise to 34 million, with 71 per cent of these likely to live in developing countries, making the need for prevention of the uncurable disease crucial. Ageing populations and increasing overweight are driving incidence of the disease upwards. The Florida researchers studied more than 1,800 older Japanese American men and women from the Kame Project in Seattle, in which participants were dementia-free at the onset of the study and were followed for up to nine years.

Dietary consumption was determined using a food frequency questionnaire given at the beginning of the study that provided information on intake of fruits, vegetables, tea, wine, and fruit and vegetable juices. The accumulation of reactive oxygen species in the brain are thought to exhaust antioxidant capacity and lead to the onset or progression of Alzheimer’s. Antioxidant vitamins, particularly vitamin E from dietary fruits and vegetables, has been associated with delayed onset of the disease, although there is little evidence to date that supplements can offer the same benefit. But animal studies have found that a number of polyphenols from juices have stronger protection for neuronal cells against oxidation than vitamins E and C. "These findings suggest that something as simple as incorporating more fruit and vegetable juices into our diet may have a significant impact on our brain health, " Borenstein said. The results could lead to a new avenue of inquiry in the prevention of Alzheimer’s, the researchers added. Another poster presentation at the conference found that moderate alcohol consumption could also influence onset of the disease, confirming previous studies showing a benefit from wine in particular. Author Mark Sager from the University of Wisconsin-Madison medical school said: "These findings contribute to the growing body of evidence that health and lifestyle variables in middle age may be associated with the subsequent risk of developing Alzheimer's in later life."

http://www.afja.com.au/news/144


 

 



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