Abstract
Parkinson's disease (PD) is one of the most common neurodegenerative diseases. Research has recently found that both animal models and patients with PD have circadian dysfunction, accompanied by abnormal expression of circadian genes and proteins, which implies that the circadian clock plays a crucial role in PD etiopathogenesis. In addition, a strong relationship between NLRP3 inflammasome signaling and PD has been observed. Meanwhile, the activation of the NLRP3 inflammasome is highly relevant to dysfunctions of the molecular clock. Therefore, alleviating the neuroinflammation caused by NLRP3 inflammasome signaling by adjusting the abnormal molecular clock may be a potential strategy for preventing and treating PD. In this article, we have reviewed the potential or direct relationship between abnormalities of the circadian clock and NLRP3 inflammasome signaling in PD.