The Role of Autophagy in the Pathogenesis of Alzheimer’s Disease
LI Chunyan1, LI Xuezhi2, QIU Kaixin1, ZHU Jin2*
Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases. Histopathologically, the hallmarks of AD include amyloid plaques (SP) constituted by amyloid-βpeptide (Aβ) and neurofibrillary tangles (NFTs) primarily composed of hyperphosphorylated tau protein. Autophagy is the major intracellular degeneration pathway of aged or damaged organelles and long-lived proteins, which is critical for maintaining cellular homeostasis. Autophagy dysfunctions lead to the over-accumulation of Aβ and hyperphosphorylated tau protein in the neuron, disturbing neuronal functions and accelerating cell apoptosis. Mounting evidence suggested that defected autophagy plays an important role in the pathological process of Alzheimer’s Disease. Reducing the over-accumulation of Aβ and hyperphosphorylated tau protein via regulating autophagy could be a potential therapeutic strategy for this disease.