Mitochondrial Dysfunction in Parkinson's Disease Pathogenesis

We investigated mitochondrial function in dopaminergic neurons derived from Parkinson's disease patient iPSCs carrying PINK1 mutations. Cells exhibited impaired mitophagy, accumulation of dysfunctional mitochondria, and increased oxidative stress. Treatment with mitochondrial-targeted antioxidants partially rescued the phenotype. Proteomic analysis identified dysregulated mitochondrial quality control pathways. These findings support mitochondrial dysfunction as a central mechanism in PD and identify potential therapeutic targets for disease modification.
