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Article type: Short Communication
Authors: Roubaud Baudron, Clairea; b; c; * | Chambonnier, Luciea; b | Buissionnière, Alicea; b | Giese, Albang; b | Macrez, Nathalieb; d | Cho, Yoonb; e | Fénelon, Valérieb; f | Blaszczyk, Lucieb; f | Dubus, Pierreb; g | Lehours, Philippea; b | Mégraud, Francisa; b | Salles, Nathaliea; b; c | Varon, Christinea; b
Affiliations: [a] INSERM U853, Bordeaux, France | [b] University of Bordeaux, Bordeaux, France | [c] Pôle de gérontologie clinique, CHU Hôpitaux de Bordeaux, Bordeaux, France | [d] CNRS, Institut des Maladies Neurodégénératives, UMR 5293, Bordeaux, France | [e] CNRS, INCIA, UMR 5287, Bordeaux, France | [f] INSERM U862 Physiopathologie de la plasticité neuronale, Bordeaux, France | [g] EA 2406 Histologie et pathologie moléculaire des tumeurs, Bordeaux, France
Correspondence: [*] Correspondence to: Claire Roubaud Baudron, MD, PhD, INSERM U853, 33076 Bordeaux cedex, France. Tel.: +33 5 57 65 66 10; Fax: +33 5 57 65 62 24; E-mail: [email protected].
Abstract: There is increasing evidence to support the role of infectious agents in the progression of Alzheimer's disease (AD), especially Helicobacter pylori (H. pylori). The impact of Helicobacter infection on the brain of non-AD predisposed mice was studied. For that, C57BL/6J mice were infected by oral gavage with H. pylori SS1 (n = 6) and Helicobacter felis (H. felis) (n = 6) or not infected (n = 6) for evaluation of neuroinflammation (anti-GFAP and anti-iba1 immunohistochemistry) and amyloid-β deposition (thioflavin-S stain and anti-Aβ immunohistochemistry). After 18-month of infection, H. pylori SS1 and H. felis infection induced a strong gastric inflammation compared to non-infected mice, but did not induce brain neuroinflammation or amyloid-β deposition.
Keywords: Alzheimer's disease, dementia, GFAP, Helicobacter pylori, iba 1, neuroinflammation, thioflavin-S
DOI: 10.3233/JAD-143129
Journal: Journal of Alzheimer's Disease, vol. 45, no. 4, pp. 1045-1050, 2015
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