期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 43, 期 1, 页码 153-165出版社
IOS PRESS
DOI: 10.3233/JAD-140198
关键词
Alzheimer's disease; glycogen synthase kinase-3 beta; Helicobacter pylori; tau hyperphosphorylation
资金
- National Natural Science Foundation of China [81271403, 81261120570]
- Fundamental Research Funds for the Central Universities, HUST [2012QN133]
Abnormal hyperphosphorylation of microtubule-associated protein tau is involved in the pathogenesis of several neurodegenerative disorders including Alzheimer's disease (AD). Helicobacter pylori (H. pylori) infection has been reported to be related with a high risk of AD, but the direct laboratory evidence is lacking. Here we explored the effect of H. pylori infection on tau phosphorylation. The results showed that H. pylori filtrate induced significant tau hyperphosphorylation at several AD-related tau phosphorylation sites, such as Thr205, Thr231, and Ser404, both in mouse neuroblastoma N2a cells and rat brains with activation of glycogen synthase kinase-3 beta (GSK-3 beta). Application of GSK-3 inhibitors efficiently attenuated the H. pylori-induced tau hyperphosphorylation. Our data provide evidence supporting the role of H. pylori infection in AD-like tau pathology, suggesting that H. pylori eradication may be beneficial in the prevention of tauopathy.
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