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Helicobacter pylori filtrate induces Alzheimer-like tau hyperphosphorylation by activating glycogen synthase

Xiu-Lian Wang1, Ji Zeng2, Yang Yang3

  • 1Key Laboratory of Neurological Disease, Ministry of Education, China, and Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China Department of Pathology, Hubei University of Chinese Medicine, Wuhan, China.

Journal of Alzheimer'S Disease : JAD
|August 1, 2014
PubMed

Insights

Helicobacter pylori (H. pylori) infection triggers abnormal tau hyperphosphorylation, a hallmark of Alzheimer's disease (AD). Eradicating H. pylori may help prevent tauopathy and protect against AD-like pathology.

Area of Science:

  • Neuroscience
  • Microbiology
  • Pathology

Background:

  • Abnormal tau hyperphosphorylation is central to Alzheimer's disease (AD) pathogenesis.
  • Helicobacter pylori (H. pylori) infection is a potential risk factor for AD, but direct evidence is limited.

Purpose of the Study:

  • To investigate the direct effect of H. pylori infection on tau phosphorylation.
  • To explore the underlying molecular mechanisms linking H. pylori to tau pathology.

Main Methods:

  • Utilized mouse neuroblastoma N2a cells and rat brain models.
  • Applied H. pylori filtrate and glycogen synthase kinase-3β (GSK-3β) inhibitors.
  • Assessed tau phosphorylation at AD-related sites (Thr205, Thr231, Ser404).

Main Results:

  • H. pylori filtrate significantly induced tau hyperphosphorylation at AD-relevant sites.
  • This hyperphosphorylation was associated with GSK-3β activation.
  • GSK-3β inhibition effectively reduced H. pylori-induced tau hyperphosphorylation.

Conclusions:

  • H. pylori infection contributes to AD-like tau pathology.
  • GSK-3β is a key mediator in H. pylori-induced tau hyperphosphorylation.
  • H. pylori eradication could be a therapeutic strategy for preventing tauopathy.
Keywords:
Alzheimer's diseaseHelicobacter pyloriglycogen synthase kinase-3βtau hyperphosphorylation

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