Microbes and Alzheimer' disease: lessons from H. pylori and GUT microbiota

F Franceschi1, V Ojetti, M Candelli

  • 1Emergency Medicine, Internal Medicine and Gastroenterology, and Institute of Neurology; Fondazione Policlinico Universitario Agostino Gemelli - IRCCS, Università Cattolica del Sacro Cuore, Rome, Italy. veronica.ojetti@gmail.com.

Abstract

Insights

Helicobacter pylori (H. pylori) infection and gut dysbiosis may contribute to Alzheimer's disease (AD) pathogenesis by promoting chronic inflammation and molecular mimicry. Further research into H. pylori eradication and gut microbiota modulation is warranted for AD prevention.

Area of Science:

  • Neuroscience
  • Microbiology
  • Immunology

Background:

  • The role of microbes and chronic inflammation in Alzheimer's disease (AD) pathogenesis is increasingly recognized.
  • Helicobacter pylori (H. pylori) infection and gut microbiota alterations are implicated in chronic inflammation, potentially influencing AD.
  • Existing literature suggests a link between these factors and neurodegenerative processes.

Purpose of the Study:

  • To analyze recent studies on the role of H. pylori and gut dysbiosis in Alzheimer's disease.
  • To explore potential pathogenic mechanisms linking microbial factors to AD.
  • To provide a comprehensive overview of current research in this field.

Main Methods:

  • Review and analysis of recent animal, human, epidemiological, and in-silico studies.
  • Examination of pathogenic explanations for the observed associations.
  • Synthesis of evidence regarding microbial influence on neurodegeneration.

Main Results:

  • Multiple studies indicate a role for H. pylori and/or gut dysbiosis in AD pathogenesis.
  • These effects are primarily mediated through the promotion of systemic chronic inflammation and molecular mimicry.
  • H. pylori infection is specifically associated with poorer cognitive performance in individuals with AD.

Conclusions:

  • Bacterial involvement in neurodegeneration is supported by evidence of inflammation, molecular mimicry, and amyloid-beta (Aβ) accumulation.
  • Findings suggest potential therapeutic strategies involving H. pylori eradication and gut microbiota modulation.
  • Further clinical trials are needed to evaluate the efficacy of antibiotics, prebiotics, and probiotics in AD prevention.

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