Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra of the midbrain. In recent years, cuproptosis,a newly discovered form of programmed cell death,has gradually gained attention for its role in the pathogenesis of PD.The core mechanism of cuproptosis involves the binding of excessive copper ions to lipoylated proteins in the tricarboxylic acid (TCA) cycle,leading to abnormal protein aggregation and loss of iron-sulfur cluster proteins, thereby triggering mitochondrial proteotoxic stress.This article systematically reviews the impact of cuproptosis on key neuronal organelles-mitochondria,the endoplasmic reticulum ,and lysosomes and its molecular mechanisms.Cuproptosis exacerbates the damage and death of dopaminergic neurons by disrupting mitochondrial respiratory chain function, intensifying oxidative stress, inhibiting mitophagy, interfering with endoplasmic reticulum protein folding and calcium homeostasis, as well as impairing lysosomal acidification and the autophagy-lysosome pathway. Understanding the interactive network between cuproptosis and organelle dysfunction may provide new potential targets for PD treatment strategies.