Neurodegenerative diseases are strongly age-related and currently cannot be cured, with a surge of patient numbers in the coming decades in view of the emerging worldwide ageing population, bringing healthcare and socioeconomic challenges. Effective therapies are urgently needed, and are dependent on new aetiological mechanisms. In neurons, efficient clearance of damaged mitochondria, through the highly evolutionary conserved cellular process termed mitophagy, plays a fundamental role in mitochondrial and metabolic homeostasis, energy supply, neuronal survival, and health. Conversely, defective mitophagy leads to accumulation of damaged mitochondria and cellular dysfunction, contributing to ageing and age-predisposed neurodegeneration. Here, we discuss the contribution of defective mitophagy in these diseases, and underlying molecular mechanisms, and highlight novel therapeutics based on new discovered mitophagy-inducing strategies.

中文翻译：

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线粒体和神经保护。

神经退行性疾病与年龄密切相关，目前无法治愈，鉴于全球范围内的老龄化人口不断涌现，未来数十年患者人数将激增，带来医疗保健和社会经济挑战。迫切需要有效的治疗方法，它取决于新的病因机制。在神经元中，通过高度进化的保守细胞过程（称为线粒体），有效清除受损的线粒体，在线粒体和代谢稳态，能量供应，神经元存活和健康中起着基本作用。相反，线粒体缺陷会导致受损的线粒体积聚和细胞功能障碍，从而导致衰老和年龄易致的神经退行性变。在这里，我们讨论了线粒体缺陷在这些疾病中的贡献以及潜在的分子机制，