生物节律的异常是衰老和帕金森病(PD)的共同表现，衰老是PD发病的危险因素之一；然而，生物节律异常是否在生理性衰老向PD的转换过程发挥作用尚未明确。最近我们发现生物节律可以调节自噬，且自噬功能的下降会加重神经炎症反应等的发生，这都与PD发病是密切相关的。但是，衰老过程中生物节律的异常是否通过自噬-炎症途径加速了生理性的衰老向PD发病的转化，尚未见相关报道。因此，本项目将从动物、细胞和分子水平，分别运用不同月龄的野生型小鼠和生物钟相关基因BMAL1敲除小鼠，研究生物节律异常对自噬-炎症反应通路的调控作用，阐明生理性衰老向PD转换的可能机制。研究成果不仅有助于明确生物节律异常在PD发病中的作用，并且可能为PD治疗提供新思路。

Circadian arrhythmia is the common manifestation of aging and Parkinson disease (PD). Aging is one of the risk factors of PD; however, it remains to be determined whether circadian arrhythmia plays a role in the transition process from aging to the development of PD. Recently, our group reported that the circadian clock could regulate autophagy under physiological conditions, which played an important role in inhibiting inflammatory response. Both autophagy dysfunction and neuroinflammation are closely related to the pathogenesis of PD. But it is unclear how the circadian arrhythmia promotes the transformation from aging to PD. Therefore, our project is to investigate the potential role and mechanism of circadian arrhythmia on the regulation of autophagy-inflammation pathway during the transition from aging to PD. The research result will not only help to clarify the role of circadian arrhythmia during PD onset, but also provide a novel avenue for the treatment of PD.