DOI | Resolve DOI: https://doi.org/10.1016/j.jalz.2012.05.1556 |
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Author | Search for: Badhwar, Aman; Search for: Brown, R.1; Search for: Delaney, Christie1; Search for: Stanimirovic, D.B.1; Search for: Haqqani, Arsalan1; Search for: Hamel, Edith |
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Affiliation | - National Research Council of Canada. Human Health Therapeutics
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Format | Text, Article |
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Subject | Alzheimer's disease; amyloid precursor protein mice; pioglitazone; cerebrovascular impairment |
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Abstract | Cerebrovascular 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. |
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Publication date | 2012-07 |
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In | |
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Language | English |
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Peer reviewed | Yes |
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NPARC number | 21275162 |
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Export citation | Export as RIS |
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Report a correction | Report a correction (opens in a new tab) |
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Record identifier | 50e79eaa-a6de-455b-bb31-5c57caea16f6 |
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Record created | 2015-05-21 |
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Record modified | 2020-04-21 |
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