[S-25] シンポジウム25
オートファジーからせまるアルツハイマー病・認知症疾患

[S-25-2] タウ伝播細胞モデルにおけるリチウムのオートファジーに対する効果

^○本井 ゆみ子^1,2, Udin Mohhamad¹, 下中 翔太朗¹, Montasir Elahi¹, 服部 信孝² (1.順天堂大学医学部 認知症・診断・予防治療学講座, 2.順天堂大学医学部附属順天堂医院 脳神経内科)

The deposition of abnormally misfolded proteins, amyloid β protein (Aβ), and tau protein is pathogenic mechanisms of Alzheimer’s disease (AD). Aβ forms senile plaques, and tau aggregates forms neurofibrillary tangles. Misfolded α-synuclein is observed in dementia with lewy bodies (DLB), and aggregated α-synuclein forms Lewy bodies. Autophagy is the main conserved pathway for the degeneration of aggregated proteins, Aβ, tau, and dysfunctional organelles in the cell. α-synuclein is also degraded in autophagy. Many animal model studies have demonstrated that autophagy normally functions as the protective factor against AD, and DLB. So, the upregulation of autophagy can be favorable in AD, or DLB treatment. The cellular and molecular machineries of autophagy, their function in the pathogenesis of AD and DLB, and current drug discovery strategies will be discussed.

1989 Graduated from Sapporo Medical College
1989 -1991 Junior resident in Sapporo Medical College
1992 - 1995 Senior resident in Juntendo University School of Medicine
2012 Associate Professor in the Department of prevention, diagnosis, treatment of Dementia, Juntendo University School of Medicine
2018 A specially Appointed Professor in the Department of prevention, diagnosis, treatment of Dementia, Juntendo University School of Medicine
2019 Director of Tokyo Medical Center for Dementia