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Martin T Henrich, Wolfgang H Oertel, D James Surmeier, Fanni F Geibl
Department of Psychiatry and Psychotherapy, Philipps University Marburg, 35039, Marburg, Germany.
Department of Neurology, Philipps University Marburg, 35043, Marburg, Germany.
Mol Neurodegener. 2023 Nov 11;18(1):83. doi: 10.1186/s13024-023-00676-7.
Mitochondrial dysfunction is strongly implicated in the etiology of idiopathic and genetic Parkinson's disease (PD). However, strategies aimed at ameliorating mitochondrial dysfunction, including antioxidants, antidiabetic drugs, and iron chelators, have failed in disease-modification clinical trials. In this review, we summarize the cellular determinants of mitochondrial dysfunction, including impairment of electron transport chain complex 1, increased oxidative stress, disturbed mitochondrial quality control mechanisms, and cellular bioenergetic deficiency. In addition, we outline mitochondrial pathways to neurodegeneration in the current context of PD pathogenesis, and review past and current treatment strategies in an attempt to better understand why translational efforts thus far have been unsuccessful.
线粒体功能障碍强烈提示特发性和遗传性帕金森病（PD）的病因。然而，旨在改善线粒体功能障碍的策略，包括抗氧化剂、抗糖尿病药物和铁螯合剂，在疾病修饰临床试验中均失败。在这篇综述中，我们总结了线粒体功能障碍的细胞决定因素，包括电子传递链复合物 1 的损伤、氧化应激增加、线粒体质量控制机制紊乱和细胞生物能量缺陷。此外，我们概述了在当前 PD 发病机制背景下线粒体向神经退行性变的途径，并回顾了过去和当前的治疗策略，试图更好地理解为什么迄今为止的转化努力都没有成功。
