铜代谢异常在帕金森发病机制中的研究进展

Research advances in the pathogenesis of abnormal copper metabolism in Parkinson’s disease

帕金森病是一种与大脑铜代谢异常有关的神经退行性疾病,铜代谢异常导致α-突触核蛋白-铜络合物的错误折叠和聚集是帕金森病的重要病理标志。铜代谢是指有铜离子参与的细胞代谢过程,与帕金森病中α-突触核蛋白聚集、多巴胺代谢、线粒体功能障碍、氧化应激、铁死亡等发病机制密切相关。在本综述中,我们通过研究铜代谢异常在帕金森病中发挥病理作用的机制,描述铜发挥其毒性的分子代谢机制,以期为进一步完善作用机制和药物的开发提供依据和帮助。

Parkinson's disease is a neurodegenerative disease associated with abnormal copper metabolism in the brain,which leads to misfolding and aggregation ofα-synuclein-copper complexes,which is an important pathological sign of Parkinson's disease.Copper metabolism,i.e.,cellular metabolic processes involving copper ions,is closely related to the pathogenesis ofα-synuclein aggregation,dopamine metabolism,mitochondrial dysfunction,oxidative stress,and ferroptosis in Parkinson's disease.In this review,we summarize the molecular metabolic mechanism of copper toxicity by studying the pathological role of copper metabolism in Parkinson's disease,to support our further understanding of the mechanism of action and drug development.