Title |
Kaolin-induced chronic hydrocephalus accelerates amyloid deposition and vascular disease in transgenic rats expressing high levels of human APP
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Published in |
Fluids and Barriers of the CNS, January 2015
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DOI | 10.1186/2045-8118-12-2 |
Pubmed ID | |
Authors |
Gerald D Silverberg, Miles C Miller, Crissey L Pascale, Ilias N Caralopoulos, Yuksel Agca, Cansu Agca, Edward G Stopa |
Abstract |
Normal pressure hydrocephalus (NPH) is most common in the elderly and has a high co-morbidity with Alzheimer's disease (AD) and cerebrovascular disease (CVD). To understand the relationship between NPH, AD and CVD, we investigated how chronic hydrocephalus impacts brain amyloid-beta peptide (Aβ) accumulation and vascular pathology in an AD transgenic rodent model. Previously we showed that the altered CSF physiology produced by kaolin-hydrocephalus in older wild-type Sprague-Dawley rats increased Aβ and hyperphosphorylated Tau (Silverberg et. al. Brain Res. 2010, 1317:286-296). We postulated that hydrocephalus would similarly affect an AD rat model. |
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Mendeley readers
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