Alzheimer’s disease (AD) is a progressive, mental illness without cure. Several years of intense research on postmortem AD brains, cell and mouse models of AD have revealed that multiple cellular changes are involved in the disease process, including mitochondrial abnormalities, synaptic damage, and glial/astrocytic activation, in addition to age-dependent accumulation of amyloid beta (Aβ) and hyperphosphorylated tau (p-tau). Synaptic damage and mitochondrial dysfunction are early cellular changes in the disease process. Healthy and functionally active mitochondria are essential for cellular functioning. Dysfunctional mitochondria play a central role in aging and AD. Mitophagy is a cellular process whereby damaged mitochondria are selectively removed from cell and mitochondrial quality and biogenesis. Mitophagy impairments cause the progressive accumulation of defective organelle and damaged mitochondria in cells. In AD, increased levels of Aβ and p-tau can induce reactive oxygen species (ROS) production, causing excessive fragmentation of mitochondria and promoting defective mitophagy. The current article discusses the latest developments of mitochondrial research and also highlights multiple types of mitophagy, including Aβ and p-tau-induced mitophagy, stress-induced mitophagy, receptor-mediated mitophagy, ubiquitin mediated mitophagy and basal mitophagy. This article also discusses the physiological states of mitochondria, including fission-fusion balance, Ca²⁺ transport, and mitochondrial transport in normal and diseased conditions. Our article summarizes current therapeutic interventions, like chemical or natural mitophagy enhancers, that influence mitophagy in AD. Our article discusses whether a partial reduction of Drp1 can be a mitophagy enhancer and a therapeutic target for mitophagy in AD and other neurological diseases.

阿尔茨海默病 (AD) 是一种进行性的、无法治愈的精神疾病。对 AD 死后大脑、细胞和小鼠模型的多年深入研究表明，除了年龄依赖性积累外，疾病过程还涉及多种细胞变化，包括线粒体异常、突触损伤和神经胶质/星形细胞激活。 β 淀粉样蛋白 (Aβ) 和过度磷酸化的 tau (p-tau)。突触损伤和线粒体功能障碍是疾病过程中的早期细胞变化。健康且功能活跃的线粒体对于细胞功能至关重要。功能失调的线粒体在衰老和 AD 中起着核心作用。线粒体自噬是一种细胞过程，通过该过程，受损的线粒体被选择性地从细胞和线粒体质量和生物发生中去除。线粒体自噬损伤导致细胞内有缺陷的细胞器和受损线粒体的逐渐积累。在 AD 中，Aβ 和 p-tau 水平的增加会诱导活性氧 (ROS) 的产生，导致线粒体过度破碎并促进有缺陷的线粒体自噬。本文讨论了线粒体研究的最新进展，并重点介绍了多种类型的线粒体自噬，包括 Aβ 和 p-tau 诱导的线粒体自噬、应激诱导的线粒体自噬、受体介导的线粒体自噬、泛素介导的线粒体自噬和基础线粒体自噬。本文还讨论了线粒体的生理状态，包括裂变-融合平衡、Ca 导致线粒体过度破碎并促进有缺陷的线粒体自噬。本文讨论了线粒体研究的最新进展，并重点介绍了多种类型的线粒体自噬，包括 Aβ 和 p-tau 诱导的线粒体自噬、应激诱导的线粒体自噬、受体介导的线粒体自噬、泛素介导的线粒体自噬和基础线粒体自噬。本文还讨论了线粒体的生理状态，包括裂变-融合平衡、Ca 导致线粒体过度破碎并促进有缺陷的线粒体自噬。本文讨论了线粒体研究的最新进展，并重点介绍了多种类型的线粒体自噬，包括 Aβ 和 p-tau 诱导的线粒体自噬、应激诱导的线粒体自噬、受体介导的线粒体自噬、泛素介导的线粒体自噬和基础线粒体自噬。本文还讨论了线粒体的生理状态，包括裂变-融合平衡、Ca²⁺运输，以及正常和患病条件下的线粒体运输。我们的文章总结了当前影响 AD 线粒体自噬的治疗干预措施，如化学或天然线粒体自噬增强剂。我们的文章讨论了 Drp1 的部分减少是否可以成为线粒体自噬增强剂和 AD 和其他神经系统疾病中线粒体自噬的治疗靶点。