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

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

Author information

1
Department of Agriculture, University of Naples "Federico II", Portici, 80055, Italy.
2
Department of Food Microbiology, Istituto Zooprofilattico Sperimentale del Mezzogiorno, Portici, 80055, Italy.
3
Sequentia Biotech, Edifici CRAG, Campus UAB, Bellaterra (Cerdanyola del Vallès), Barcelona, 08193, Spain.
4
Department of Agriculture, University of Naples "Federico II", Portici, 80055, Italy. iannelli@unina.it.
5
Department of Immunology, Weizmann Institute of Science, Rehovot, 76100, Israel.
6
Department of Agriculture, University of Naples "Federico II", Portici, 80055, Italy. capparel@unina.it.

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.

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