Long term changes in phospho-APP and tau aggregation in the 3xTg-AD mice following cerebral ischemia

被引：32

作者：

Koike, M. A. ^{[1
]}

Garcia, F. G. ^{[1
]}

Kitazawa, M. ^{[1
]}

Green, K. N. ^{[1
]}

LaFerla, F. M. ^{[1
]}

机构：

[1] Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA

来源：

NEUROSCIENCE LETTERS | 2011年 / 495卷 / 01期

关键词：

Alzheimer's disease; Ischemia; Stroke; Phospho-APP; AMYLOID PRECURSOR PROTEIN; TRAUMATIC BRAIN-INJURY; ALZHEIMERS-DISEASE; A-BETA; VASCULAR-LESIONS; EXPRESSION; PLAQUES; BACE1; PHOSPHORYLATION; PREVALENCE;

D O I：

10.1016/j.neulet.2011.03.034

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

The risk of Alzheimer's disease increases following cerebral hypoperfusion. We studied the long-term interaction between low blood flow to the brain and Alzheimer's disease by inducing a transient global ischemic insult in aged 3xTg-AD mice and determining the effects on AD pathology 3-months post injury. We found that global ischemia does not increase the levels of amyloid-beta in these mice. However, the injury did lead to enhanced phosphorylation of the amyloid precursor protein (APP) at the Thr668 site in both the 3xTg-AD mice and wild-type controls. Furthermore, we found an increase in insoluble total tau 3-months post-injury. Together these findings further elucidate the long-term impact of cerebral hypoperfusion on Alzheimer's disease. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

引用

页码：55 / 59

页数：5

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