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.

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.

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.

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.