Affiliations: [a] Key Laboratory of Neurological Disease, Ministry of Education, China, and Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China | [b] Department of Clinical Laboratory, Wuhan Pu Ai Hospital, Huazhong University of Science and Technology, Wuhan, China | [c] Department of Pathology, Hubei University of Chinese Medicine, Wuhan, China
Correspondence:
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Correspondence to: Rong Liu and Jian-Zhi Wang, Key Laboratory of Neurological Disease, Ministry of Education, China, and Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Tel./Fax: +86 027 83693883; E-mails: rong.liu@hust.edu.cn, wangjz@mails.tjmu.edu.cn.
Note: [1] These authors contribute equally to this work.
Abstract: 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-3β (GSK-3β). 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.
Keywords: Alzheimer's disease, glycogen synthase kinase-3β, Helicobacter pylori, tau hyperphosphorylation
