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
--
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
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
