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Central angiotensin II‐induced Alzheimer‐like tau phosphorylation in normal rat brains
Author(s) -
Tian Minjie,
Zhu Donglin,
Xie Wei,
Shi Jingping
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.09.004
Subject(s) - angiotensin ii , mediator , gsk 3 , losartan , alzheimer's disease , neurotoxicity , glycogen synthase , endocrinology , phosphorylation , medicine , kinase , tau protein , neuroscience , chemistry , biology , microbiology and biotechnology , disease , toxicity , receptor
Growing evidence suggests that Alzheimer disease (AD) origins in vascular lesions. As the crucial mediator of vascular pathology, angiotensin II‐induced significant amyloid production in our laboratory, although amyloid neurotoxicity depended on phosphorylated tau (p‐tau) in recent studies. In the present study, p‐tau levels were significantly elevated by central angiotensin II via glycogen synthase kinase 3β (GSK 3β) and other tau kinases. Moreover, angiotensin II‐induced cognitive impairment and tau phosphorylation was attenuated by losartan and a GSK 3β inhibitor. These findings implicate Ang II as a crucial mediator of AD pathology and a link between cardiovascular events and AD.