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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6815
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pubmed:dateCreated |
2001-1-3
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pubmed:abstractText |
Much evidence indicates that abnormal processing and extracellular deposition of amyloid-beta peptide (A beta), a proteolytic derivative of the beta-amyloid precursor protein (betaAPP), is central to the pathogenesis of Alzheimer's disease (reviewed in ref. 1). In the PDAPP transgenic mouse model of Alzheimer's disease, immunization with A beta causes a marked reduction in burden of the brain amyloid. Evidence that A beta immunization also reduces cognitive dysfunction in murine models of Alzheimer's disease would support the hypothesis that abnormal A beta processing is essential to the pathogenesis of Alzheimer's disease, and would encourage the development of other strategies directed at the 'amyloid cascade'. Here we show that A beta immunization reduces both deposition of cerebral fibrillar A beta and cognitive dysfunction in the TgCRND8 murine model of Alzheimer's disease without, however, altering total levels of A beta in the brain. This implies that either a approximately 50% reduction in dense-cored A beta plaques is sufficient to affect cognition, or that vaccination may modulate the activity/abundance of a small subpopulation of especially toxic A beta species.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:issn |
0028-0836
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pubmed:author |
pubmed-author:BergeronCC,
pubmed-author:ChishtiM AMA,
pubmed-author:FraserP EPE,
pubmed-author:FrenchJJ,
pubmed-author:HeslinDD,
pubmed-author:HornePP,
pubmed-author:JanusCC,
pubmed-author:JiangYY,
pubmed-author:MathewsP MPM,
pubmed-author:McLaurinJJ,
pubmed-author:MerckenMM,
pubmed-author:MountH THT,
pubmed-author:NixonR ARA,
pubmed-author:PearsonJJ,
pubmed-author:SchmidtS DSD,
pubmed-author:St George-HyslopPP,
pubmed-author:WestawayDD
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pubmed:issnType |
Print
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pubmed:volume |
408
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
979-82
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11140685-Alzheimer Disease,
pubmed-meshheading:11140685-Amyloid,
pubmed-meshheading:11140685-Amyloid beta-Peptides,
pubmed-meshheading:11140685-Animals,
pubmed-meshheading:11140685-Cricetinae,
pubmed-meshheading:11140685-Disease Models, Animal,
pubmed-meshheading:11140685-Hippocampus,
pubmed-meshheading:11140685-Humans,
pubmed-meshheading:11140685-Islet Amyloid Polypeptide,
pubmed-meshheading:11140685-Maze Learning,
pubmed-meshheading:11140685-Mesocricetus,
pubmed-meshheading:11140685-Mice,
pubmed-meshheading:11140685-Mice, Inbred C3H,
pubmed-meshheading:11140685-Mice, Transgenic,
pubmed-meshheading:11140685-Peptide Fragments,
pubmed-meshheading:11140685-Plaque, Amyloid,
pubmed-meshheading:11140685-Vaccination
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pubmed:articleTitle |
A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease.
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pubmed:affiliation |
Centre for Research in Neurodegenerative Diseases, Department of Medicine, University of Toronto, Ontario, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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