DOI | Trouver le DOI : https://doi.org/10.1016/j.jalz.2012.05.1556 |
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Auteur | Rechercher : Badhwar, Aman; Rechercher : Brown, R.1; Rechercher : Delaney, Christie1; Rechercher : Stanimirovic, D.B.1; Rechercher : Haqqani, Arsalan1; Rechercher : Hamel, Edith |
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Affiliation | - Conseil national de recherches du Canada. Thérapeutique en santé humaine
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Format | Texte, Article |
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Sujet | Alzheimer's disease; amyloid precursor protein mice; pioglitazone; cerebrovascular impairment |
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Résumé | 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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Date de publication | 2012-07 |
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Dans | |
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Langue | anglais |
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Publications évaluées par des pairs | Oui |
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Numéro NPARC | 21275162 |
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Exporter la notice | Exporter en format RIS |
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Signaler une correction | Signaler une correction (s'ouvre dans un nouvel onglet) |
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Identificateur de l’enregistrement | 50e79eaa-a6de-455b-bb31-5c57caea16f6 |
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Enregistrement créé | 2015-05-21 |
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Enregistrement modifié | 2020-04-21 |
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