NEURO61

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

Tue. Sep 1, 2020 9:00 AM - 10:30 AM Room 10 (Okayama Prefectural Medical Association 2F miki anniversary Hall)

Chair：YumikoMotoi（Juntendo University School of Medicine, Dept of Diagnosis, Prevention, and Treatment of Dementia）,TadanoriHamano（Department of Neurology, University of Fukui）

[S-25-1] Degradation of amyloid ß protein and tau in Autophagy

○Tadanori Hamano (Department of Neurology, University of Fukui, 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.

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

○Yumiko Motoi1,2, 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.

[S-25-3] Granulovacuolar degeneration in neurodegeneration

○Koki Makioka1, Tsuneo Yamazaki2, Masamitsu Takatama3, Koichi Okamoto3, Yoshio Ikeda1 (1.Department of Neurology, Gunma University Graduate School of Medicine, Japan, 2.Gunma University School of Health Sciences, Japan, 3.Geriatrics Research Institute and Hospital, 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.

[S-25-4] Alteration of autophagy-related proteins in synucleinopathies

○Yasuo Miki (Department of Neuropathology, Hirosaki University Graduate School of Medicine, 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.