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FEBS Lett. 2012 Oct 19;586(20):3737-45. doi: 10.1016/j.febslet.2012.09.004. Epub 2012 Sep 13.

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

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1
Department of Neurology, Nanjing Brain Hospital Affiliated to Nanjing Medical University, Nanjing, PR China.

Erratum in

  • FEBS Lett. 2013 Mar 18;587(6):818.

Abstract

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.

PMID:
22982863
DOI:
10.1016/j.febslet.2012.09.004
[Indexed for MEDLINE]
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