Abstract:

Age-related neurodegenerative diseases is increasing with the aggravation of global aging. Studies show that neurodegenerative diseases could be prevented or delayed by intermittent fasting (IF) regulating metabolic pathways, and the mechanism of action may be associated with improved mitochondrial function and metabolic homeostasis by IF. Mitochondrial dysfunction is an early marker of brain aging and neurodegeneration. These suggest that IF, mitochondria, and neurodegenerative diseases may be closely correlated. We reviewed the improvement effects of IF on neurodegenerative diseases, the important role of mitochondria in neurodegenerative diseases, the regulation of IF on mitochondrial function, and the effects of excessive calorie intake on neurons and mitochondrial function, and summarized that IF could improve mitochondrial function, while excessive calorie intake could damage the neurons and mitochondrial function. Future research could continue to focus on the mechanism of action and metabolism signal pathway of IF improving neurodegenerative diseases, which may be favorable to the determination of the proper window period for intervention, and the development of alternative targeted drug therapy, thereby assisting clinical application of IF.

Key words: Mitochondria, Intermittent fasting, Neurodegenerative diseases, Aging, Review

摘要：

伴随世界人口老龄化的加剧，以衰老为主要危险因素的神经退行性疾病发病率日渐升高。间歇性禁食（IF）通过调节代谢途径来预防或延缓神经退行性疾病已有研究，其机制可能与IF可以调节线粒体功能及内环境稳态有关，而线粒体功能障碍是脑老化和神经退行性变的早期特征。这些提示IF、线粒体与神经退行性疾病存在密切联系。本文就IF对神经退行性疾病的改善作用、线粒体在神经退行性疾病中发挥重要作用、IF对线粒体功能的调节以及过量热量摄入对神经元及线粒体的影响4个方面，从正反角度进行综述，分析得出IF可以调节线粒体功能、过量热量摄入可能损伤神经元及线粒体功能，并认为后期可进一步深入研究IF改善神经退行性疾病的具体机制及其对神经系统代谢转变的具体信号通路，进而判断最佳干预时间，开发更有靶向性的药物替代疗法，从而帮助IF研究成果的临床转化。

关键词: 线粒体, 间歇性禁食, 神经退行性疾病, 衰老, 综述