[S-25] Symposium 25
The Implication of Autophagy in Alzheimer's disease and Dementia

[S-25-2] A Role of Lithium on Autophagy in Tau Propagation Cell Models

^○Yumiko Motoi^1,2, Udin Mohhamad¹, Shotaro Shimonaka¹, Montasir Elahi¹, Nobutaka Hattori² (1.Juntendo University, Dept. of Diagnosis, Prevention, and Treatment of Dementia, Japan, 2.Juntendo University, Dept. of Neurology, Japan)

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