TY - JOUR
T1 - Microbes and Alzheimer' disease: Lessons from H. Pylori and GUT microbiota
AU - Franceschi, Francesco
AU - Ojetti, Veronica
AU - Candelli, Marcello
AU - Covino, Marcello
AU - Cardone, S.
AU - Potenza, Angelo Eugenio
AU - Simeoni, Benedetta
AU - Gabrielli, Maurizio
AU - Sabia, Luca
AU - Gasbarrini, Giovanni Battista
AU - Lopetuso, Loris Riccardo
AU - Scaldaferri, Franco
AU - Rossini, Paolo Maria
AU - Gasbarrini, Antonio
PY - 2019
Y1 - 2019
N2 - 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 Aß 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.
AB - 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 Aß 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.
KW - Alzheimer' disease
KW - Amyloid
KW - H. pylori
KW - Inflammation
KW - Microbiota
KW - Molecular mimicry
KW - Pharmacology (medical)
KW - Alzheimer' disease
KW - Amyloid
KW - H. pylori
KW - Inflammation
KW - Microbiota
KW - Molecular mimicry
KW - Pharmacology (medical)
UR - http://hdl.handle.net/10807/131088
UR - https://www.europeanreview.org/wp/wp-content/uploads/426-430-1.pdf
U2 - 10.26355/eurrev_201901_16791
DO - 10.26355/eurrev_201901_16791
M3 - Article
SN - 1128-3602
VL - 23
SP - 426
EP - 430
JO - European Review for Medical and Pharmacological Sciences
JF - European Review for Medical and Pharmacological Sciences
ER -