Central angiotensin II-induced Alzheimer-like tau phosphorylation in normal rat brains

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 3 beta (GSK 3 beta) and other tau kinases. Moreover, angiotensin II-induced cognitive impairment and tau phosphorylation was attenuated by losartan and a GSK 3 beta inhibitor. These findings implicate Ang II as a crucial mediator of AD pathology and a link between cardiovascular events and AD. (c) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.