阿尔茨海默病 (AD) 和帕金森病 (PD) 等神经退行性疾病 (NDD) 是一组以神经元进行性退化为特征的异质性疾病。NDDs 威胁着全世界数百万人的生命，令人遗憾的是仍然无法治愈。人们普遍认为，线粒体功能障碍是 NDDs 发病机制的基础。线粒体功能障碍导致能量耗竭、氧化应激、钙超载、半胱天冬酶激活，这些是导致 NDD 神经元死亡的主要原因。因此，线粒体是 NDDs 干预的首选靶点。到目前为止，已经开发出各种靶向线粒体的药物，其中一些令人欣喜地显示出有希望的结果，尽管仍然存在一些障碍，例如靶向特异性、递送能力阻碍了药物的开发。在本综述中，我们将详细阐述 1）线粒体靶向药物的设计策略，2）各个线粒体靶向药物的拯救机制，3）如何评估治疗效果。希望这篇综述能为了解如何开发更有效的治疗 NDD 的药物提供全面的知识。

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Neurodegenerative diseases (NDDs) such as Alzheimer's disease (AD) and Parkinson's disease (PD) are a heterogeneous group of disorders characterized by progressive degeneration of neurons. NDDs threaten the lives of millions of people worldwide and regretfully remain incurable. It is well accepted that dysfunction of mitochondria underlies the pathogenesis of NDDs. Dysfunction of mitochondria results in energy depletion, oxidative stress, calcium overloading, caspases activation, which dominates the neuronal death of NDDs. Therefore, mitochondria are the preferred target for intervention of NDDs. So far various mitochondria-targeting drugs have been developed and delightfully some of them demonstrate promising outcome, though there are still some obstacles such as targeting specificity, delivery capacity hindering the drugs development. In present review, we will elaborately address 1) the strategy to design mitochondria targeting drugs, 2) the rescue mechanism of respective mitochondria targeting drugs, 3) how to evaluate the therapeutic effect. Hopefully this review will provide comprehensive knowledge for understanding how to develop more effective drugs for the treatment of NDDs.