Zhang Yao, Li Xiao-Wen, Zhang Yuan, Li Xing
National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, Key Laboratory of Medicinal Resources and Natural Pharmaceutical Chemistry (Shaanxi Normal University), The Ministry of Education, College of Life Sciences, Shaanxi Normal University, Xi'an, 710119, Shaanxi, China.
J Neurol. 2025 Apr 28;272(5):364. doi: 10.1007/s00415-025-13101-4.
Given the high energy demand of the nervous system, mitochondrial dysfunction is a key factor in the pathogenesis of neurodegenerative diseases. Thus, a comprehensive understanding of its mechanisms and potential therapeutic targets is essential. This review discusses the roles of mitochondrial oxidative stress, mitochondrial dynamics alterations, and mtDNA damage in Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and multiple sclerosis (MS). In addition, it summarizes the contributions of novel technological approaches in detecting mitochondrial dysfunction, which assist in disease diagnosis. We also emphasize emerging therapeutic strategies and drugs aimed at enhancing mitochondrial quality control and reducing oxidative stress, thereby laying the groundwork for innovative therapeutic approaches in neurodegenerative disease treatment.
鉴于神经系统对能量的高需求，线粒体功能障碍是神经退行性疾病发病机制中的关键因素。因此，全面了解其机制和潜在治疗靶点至关重要。本综述讨论了线粒体氧化应激、线粒体动力学改变和线粒体DNA损伤在阿尔茨海默病（AD）、帕金森病（PD）、亨廷顿病（HD）和多发性硬化症（MS）中的作用。此外，还总结了用于检测线粒体功能障碍的新技术方法在疾病诊断中的作用。我们还强调了旨在增强线粒体质量控制和降低氧化应激的新兴治疗策略和药物，从而为神经退行性疾病治疗中的创新治疗方法奠定基础。
