Alzheimer's disease (AD) is an age-dependent, incurable mental illness that is associated with the accumulation of aggregates of amyloid-beta (Aβ) and hyperphosphorylated tau fragments (p-tau). Detailed studies on postmortem AD brains, cell lines, and mouse models of AD have shown that numerous cellular alterations, including mitochondrial deficits, synaptic disruption and glial/astrocytic activation, are involved in the disease process. Mitophagy is a cellular process by which damaged/weakened mitochondria are selectively eliminated from the cell. In AD, impairments in mitophagy trigger the gradual accumulation of defective mitochondria. This review will focus on the recent progress in understanding the molecular mechanisms and pathological role of mitophagy and its implications for AD pathogenesis. We will also discuss the novel concept of the regulation of mitophagy as a therapeutic avenue for the prevention and treatment of AD.

阿尔茨海默病 (AD) 是一种与年龄相关的无法治愈的精神疾病，与β-淀粉样蛋白 (Aβ) 和过度磷酸化 tau 片段 (p-tau) 聚集体的积累有关。对死后 AD 大脑、细胞系和 AD 小鼠模型的详细研究表明，许多细胞改变，包括线粒体缺陷、突触破坏和神经胶质/星形胶质细胞激活，都与疾病过程有关。线粒体自噬是一种细胞过程，通过该过程，受损/弱化的线粒体被选择性地从细胞中清除。在 AD 中，线粒体自噬的损伤会引发缺陷线粒体的逐渐积累。本综述将重点介绍了解线粒体自噬的分子机制和病理作用及其对 AD 发病机制的影响的最新进展。