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

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 g...

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Bibliographic Details
Published in:Scientific reports 2017-08, Vol.7 (1), p.7817-14, Article 7817
Main Authors: Contaldi, Felice, Capuano, Federico, Fulgione, Andrea, Aiese Cigliano, Riccardo, Sanseverino, Walter, Iannelli, Domenico, Medaglia, Chiara, Capparelli, Rosanna
Format: Article
Language:English
Subjects:
45
45/90
45/91
631/378/1689/1283
631/378/2649/2150
Alzheimer Disease - genetics
Alzheimer Disease - microbiology
Apolipoprotein E
Bacterial Proteins - pharmacology
Cell Line
Disease
Disease Susceptibility
Gastric Mucosa - chemistry
Gastric Mucosa - cytology
Gastric Mucosa - drug effects
Gene expression
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
Humanities and Social Sciences
Humans
multidisciplinary
Neurological diseases
Peptide Fragments - pharmacology
Science
Science (multidisciplinary)
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Summary: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.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-017-07532-x