The role of microbial amyloid in neurodegeneration

演 者

Robert P. Friedland, MD(ルイビル大学医学部神経内科学講座教授)

日 時


場 所

基礎研究棟2階 教職員ロビー


It has become apparent that the intestinal microbiota orchestrate important aspects of our metabolism, immunity and development. Recent work has demonstrated that the microbiota also influence brain function in healthy and diseased individuals. Of great interest are reports that intestinal bacteria play a role in the pathogenic cascade of both Parkinson's and Alzheimer's diseases. Recent work also suggests that inflammasome activation may be the cause of amyloid beta aggregation in Alzheimer's disease. Neurodegenerative disorders involve misfolding of endogenous proteins which spreads from one region of the body to another in a manner analogous to prions. Sterile neuroinflammation is also observed. The mechanisms of how the microbiota influences disease requires elaboration. Microbial proteins or metabolites may influence neurodegeneration through promotion of amyloid formation by human proteins or by enhancing inflammatory responses to endogenous neuronal amyloids. Current knowledge concerning bacterial amyloids illustrates their potential to influence cerebral amyloid aggregation as well as neuroinflammation. The term “mapranosis” is proposed to describe microbiota-associated proteopathy and neuroinflammation. The study of amyloid proteins made by the microbiota and their influence on health and disease is in its infancy. This is a promising area for therapeutic intervention, as there are many ways to alter our microbial partners and their products, including amyloid proteins.

神経難病研究センター神経診断治療学部門・実験実習支援センター 共催


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