The hypothesis that Helicobacter pylori predisposes to Alzheimer's disease is biologically plausible

Sci Rep. 2017 Aug 10;7(1):7817. doi: 10.1038/s41598-017-07532-x.

Abstract

There is epidemiological evidence that H. pylori might predispose to Alzheimer's disease. To understand the cellular processes potentially linking such unrelated events, we incubated the human gastric cells MNK-28 with the H. pylori peptide Hp(2-20). We then monitored the activated genes by global gene expression. The peptide modulated 77 genes, of which 65 are listed in the AlzBase database and include the hallmarks of Alzheimer's disease: APP, APOE, PSEN1, and PSEN2. A large fraction of modulated genes (30 out of 77) belong to the inflammation pathway. Remarkably, the pathways dis-regulated in Alzheimer's and Leasch-Nyhan diseases result dis-regulated also in this study. The unsuspected links between such different diseases - though still awaiting formal validation - suggest new directions for the study of neurological diseases.

MeSH terms

  • Alzheimer Disease / genetics
  • Alzheimer Disease / microbiology
  • Bacterial Proteins / pharmacology*
  • Cell Line
  • Disease Susceptibility
  • Gastric Mucosa / chemistry
  • Gastric Mucosa / cytology*
  • Gastric Mucosa / drug effects
  • Gene Expression Profiling / methods
  • Gene Expression Regulation / drug effects
  • Gene Regulatory Networks / drug effects*
  • Helicobacter Infections / complications
  • Helicobacter Infections / genetics
  • Helicobacter pylori / metabolism*
  • Helicobacter pylori / pathogenicity
  • Humans
  • Peptide Fragments / pharmacology*

Substances

  • Bacterial Proteins
  • Hp (2-20) protein, Helicobacter pylori
  • Peptide Fragments