Affiliations: [a] University of Bordeaux, UMR BaRITOn, INSERM 1053, Bordeaux, France
| [b] CHU Bordeaux, Pôle de Gérontologie Clinique, Bordeaux, France
| [c]
University of Bordeaux, NutriNeuro, INRA 1286, Bordeaux, France
| [d] CHU Bordeaux, Service de biologie des tumeurs - tumorothèque, Bordeaux, France
| [e]
French National Reference Center for Campylobacters & Helicobacters, Bordeaux, France
Correspondence:
[*]
Correspondence to: Claire Roubaud-Baudron, MD, PhD, Hôpital Xavier Arnozan, CHU de Bordeaux, Avenue du
Haut Leveque, 33604 Pessac Cedex, France. Tel.: +33 (0) 5 57 65 65 57; Fax: +33 (0) 5 57 65 65 60;
E-mail: [email protected].
Abstract: Despite extensive research, the origin of Alzheimer’s disease (AD) remains unknown. The role of infectious pathogens has recently emerged. Epidemiological studies have shown that Helicobacter pylori infection increases the risk of developing AD. We hypothesized that H. pylori-induced gastritis may be associated with a systemic inflammation and finally neuroinflammation. C57BL/6 mice were infected with H. pylori (n = 15) or Helicobacter felis (n = 13) or left uninfected (n = 9) during 18 months. Gastritis, amyloid deposition, astroglial and microglial cell area, and systemic and brain cytokines were assessed. The infection (H. felis> H. pylori) induced a severe gastritis and an increased neuroinflammation but without brain amyloid deposition or systemic inflammation.
