Modifiable risk factors for Alzheimer's disease and glia-driven neuroinflammation:
what are the links?

− この都医学研セミナーは終了しました。 −

演者 Andis Klegeris
Laboratory of Cellular and Molecular Pharmacology, University of British Columbia Okanagan Campus, Canada(Associate Professor)
会場 東京都医学総合研究所 2BC会議室
日時 平成30年6月25日(月)14:30~
世話人 細川 雅人 (認知症プロジェクト)
参加自由 詳細は下記問合せ先まで
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Currently, there are no effective treatment options for Alzheimer’s disease; therefore, elucidating strategies for delaying or preventing this debilitating neurodegenerative disease is an emerging area of research. There are several well-established modifiable risk factors for Alzheimer's disease including obesity, type 2 diabetes and physical inactivity. These processes are known to alter peripheral immune responses, but their interaction with neuroimmune mechanisms are not well understood. We have observed interactions of several molecules associated with the above risk factors with non-neuronal glial cells of the brain. Direct signaling between the periphery and glia, which orchestrate neuroinflammatory responses, could be responsible for the altered risk of Alzheimer's disease. Characterization of such neuroimmune regulation could identify new therapeutic targets for delaying or slowing Alzheimer's disease process.