假设幽门螺杆菌易患阿尔茨海默病在生物学上是合理的。

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

机构信息

Department of Agriculture, University of Naples "Federico II", Portici, 80055, Italy.

Department of Food Microbiology, Istituto Zooprofilattico Sperimentale del Mezzogiorno, Portici, 80055, Italy.

出版信息

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

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.

有流行病学证据表明，幽门螺杆菌可能使阿尔茨海默病更容易发生。为了了解可能将这些不相关事件联系起来的细胞过程，我们将人类胃细胞 MNK-28 与幽门螺杆菌肽 Hp(2-20)一起孵育。然后，我们通过全基因表达监测激活的基因。该肽调节了 77 个基因，其中 65 个列在 AlzBase 数据库中，包括阿尔茨海默病的特征：APP、APOE、PSEN1 和 PSEN2。大量被调节的基因（77 个中的 30 个）属于炎症途径。值得注意的是，在阿尔茨海默病和 Leasch-Nyhan 病中失调的途径在本研究中也失调。尽管仍有待正式验证，但这些不同疾病之间意想不到的联系表明了神经系统疾病研究的新方向。