Artículo Materias > Alimentación Universidad Europea del Atlántico > Investigación > Artículos y libros
Universidad Internacional Iberoamericana México > Investigación > Producción Científica
Universidad Internacional Iberoamericana Puerto Rico > Investigación > Producción Científica Abierto Inglés It has been hypothesized that alterations in the composition of the gut microbiota might be associated with the onset of certain human pathologies, such as Alzheimer disease, a neurodegenerative syndrome associated with cerebral accumulation of amyloid-β fibrils. It has been shown that bacteria populating the gut microbiota can release significant amounts of amyloids and lipopolysaccharides, which might play a role in the modulation of signaling pathways and the production of proinflammatory cytokines related to the pathogenesis of Alzheimer disease. Additionally, nutrients have been shown to affect the composition of the gut microbiota as well as the formation and aggregation of cerebral amyloid-β. This suggests that modulating the gut microbiome and amyloidogenesis through specific nutritional interventions might prove to be an effective strategy to prevent or reduce the risk of Alzheimer disease. This review examines the possible role of the gut in the dissemination of amyloids, the role of the gut microbiota in the regulation of the gut–brain axis, the potential amyloidogenic properties of gut bacteria, and the possible impact of nutrients on modulation of microbiota composition and amyloid formation in relation to the pathogenesis of Alzheimer disease. metadata Pistollato, Francesca; Sumalla Cano, Sandra; Elío Pascual, Iñaki; Masias Vergara, Manuel; Giampieri, Francesca y Battino, Maurizio mail francesca.pistollato@uneatlantico.es, sandra.sumalla@uneatlantico.es, inaki.elio@uneatlantico.es, manuel.masias@uneatlantico.es, francesca.giampieri@uneatlantico.es, maurizio.battino@uneatlantico.es (2016) Role of gut microbiota and nutrients in amyloid formation and pathogenesis of Alzheimer disease. Nutrition Reviews, 74 (10). pp. 624-634. ISSN 0029-6643