Abstract:Parkinson’s disease is a neurodegenerative disease associated with abnormal copper metabolism in the brain, which leads to misfolding and aggregation of α-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 of α-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.