Microbes and Alzheimer’ disease: lessons from H. pylori and GUT microbiota

F. Franceschi, V. Ojetti, M. Candelli, M. Covino, S. Cardone, A. Potenza, B. Simeoni, M. Gabrielli, L. Sabia, G. Gasbarrini, L. Lopetuso, F. Scaldaferri, P.M. Rossini, A. Gasbarrini

Emergency Medicine, Internal Medicine and Gastroenterology, and Institute of Neurology; Fondazione Policlinico Universitario Agostino Gemelli – IRCCS, Università Cattolica del Sacro Cuore, Rome, Italy. veronica.ojetti@gmail.com

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• Pharmacology

OBJECTIVE: the role of microbes and chronic inflammation in the pathogenesis of Alzheimer’ disease (AD) has been postulated by many authors. On the other hand, several studies have reported the main role of H. pylori infection and/or GUT microbiota alteration in promoting chronic inflammation, thus possibly influencing both occurrence and evolution of AD. In this article, we analyze the most important and recent studies performed on this field both on humans and animals and provide possible pathogenic explanations.

RESULTS: all main and most recent animal, human, epidemiological and in-silico studies, showed a role of H. pylori and/or dysbiosis in AD, mostly through the promotion of systemic chronic inflammation and/or by triggering molecular mimicry mechanisms. In particular, H. pylori infection seems to be related to a poorer cognitive performance.

CONCLUSIONS: Indeed, bacteria have been shown to affect neurodegeneration by promoting inflammation, inducing molecular mimicry mechanisms and accumulation of Aβ into the brain. These findings open the way for H. pylori eradicating trials and/or GUT microbiota remodulating strategies. Therefore, further studies are now needed in order to test whether antibiotics, pre and/or probiotics may exert a beneficial effect in the prevention of AD.

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