In addition to ATP synthesis, mitochondria are highly dynamic organelles that modulate apoptosis, ferroptosis, and inflammasome activation. Through executing these varied functions, the mitochondria play critical roles in the development and progression of neurodegenerative diseases including Alzheimer disease, Parkinson disease, Huntington disease, and Friedreich ataxia, among others. Impaired mitochondrial biogenesis and abnormal mitochondrial dynamics contribute to mitochondrial dysfunction in these diseases. Additionally, dysfunctional mitochondria play critical roles in signaling for both inflammasome activation and ferroptosis. Therapeutics are being developed to circumvent inflammasome activation and ferroptosis in dysfunctional mitochondria. Targeting these aspects of mitochondrial dysfunction may present viable therapeutic strategies for combatting the neurodegenerative diseases. This review aims to summarize the role of the mitochondria in the development and progression of neurodegenerative diseases and to present current therapeutic approaches that target mitochondrial dysfunction in these diseases.

除ATP合成外，线粒体是高动态细胞器，可调节细胞凋亡，肥大症和炎症小体活化。通过执行这些不同的功能，线粒体在神经退行性疾病（包括阿尔茨海默氏病，帕金森氏病，亨廷顿病和弗雷德里希共济失调等）的发生和发展中起关键作用。线粒体生物发生受损和线粒体动力学异常导致这些疾病中的线粒体功能障碍。此外，功能失调的线粒体在炎症小体激活和肥大症的信号传递中也起着关键作用。正在开发治疗剂来绕过功能异常的线粒体中的炎性体活化和肥大症。针对线粒体功能障碍的这些方面，可能会提出与神经退行性疾病作斗争的可行治疗策略。这篇综述旨在总结线粒体在神经退行性疾病的发展和进程中的作用，并提出针对这些疾病中线粒体功能障碍的当前治疗方法。