Rescue of beta-amyloid–induced alterations in cerebrovascular protein expression by pioglitazone in APP mice: Link to functional recovery in the cerebrovasculature

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DOIResolve DOI: http://doi.org/10.1016/j.jalz.2012.05.1556
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TypeArticle
Journal titleAlzheimer's and Dementia
ISSN1552-5260
Volume8
Issue4
Article numberSupplement
PagesP574P575
SubjectAlzheimer's disease; amyloid precursor protein mice; pioglitazone; cerebrovascular impairment
AbstractCerebrovascular dysfunction appears prior to Aβ-plaque deposition and measurable mnemonic impairment in Alzheimer's disease (AD) patients and amyloid precursor protein (APP)-expressing transgenic mice. The soluble, highly toxic Aβ-fragment generated from the amyloidogenic processing of APP is likely the primary instigator of chronic cerebrovascular insufficiency in APP mice. We recently demonstrated that the PPAR-gamma agonist, pioglitazone, is a potent drug for reversing cerebrovascular impairment at all stages of Aβ-induced pathology in APP mice. Our aims are to (a) characterize the effect of Aβ-overproduction on the cerebrovascular proteome of APP mice; (b) determine the extent to which pioglitazone rescues the Aβ-altered cerebrovascular proteome; and (c) determine the link between protein expression rescue by pioglitazone and functional recovery in the cerebrovasculature.
Publication date
LanguageEnglish
AffiliationHuman Health Therapeutics; National Research Council Canada
Peer reviewedYes
NPARC number21275162
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Record identifier50e79eaa-a6de-455b-bb31-5c57caea16f6
Record created2015-05-21
Record modified2016-05-09
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