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

被引：25

作者：

Felice, Contaldi ^{[1
]}

Federico, Capuano ^{[2
]}

Andrea, Fulgione ^{[1
]}

Cigliano Riccardo, Aiese ^{[3
]}

Walter, Sanseverino ^{[3
]}

Domenico, Iannelli ^{[1
]}

Chiara, Medaglia ^{[4
]}

Rosanna, Capparelli ^{[1
]}

机构：

[1] Univ Naples Federico II, Dept Agr, I-80055 Portici, Italy

[2] Ist Zooprofilatt Sperimentale Mezzogiorno, Dept Food Microbiol, I-80055 Portici, Italy

[3] Sequentia Biotech, Edifici CRAG,Campus UAB, Barcelona 08193, Spain

[4] Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel

来源：

SCIENTIFIC REPORTS | 2017年 / 7卷

关键词：

BLOOD-BRAIN-BARRIER; NITRIC-OXIDE SYNTHASE; APOLIPOPROTEIN-E; GENOME-WIDE; IN-VITRO; RNA-SEQ; PEPTIDE; GENE; EXPRESSION; RISK;

D O I：

10.1038/s41598-017-07532-x

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页数：14

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