Mitochondrial dysfunction in Parkinson's disease and aging

Parkinson's disease (PD) is a neurodegenerative disorder for which advancing age is the major risk factor. Aging and PD share several features, including chronic neuroinflammation and pathological protein accumulation. This overlap suggests that mechanisms driving the aging process may also contribute to the onset and progression of PD. In this narrative review, we examine mitochondrial dysfunction as a shared feature of aging and PD, focusing on energy production, calcium buffering, apoptosis, inflammation, and reactive oxygen species (ROS) generation. The literature reviewed here suggests shared alterations in mitochondrial dynamics, increased mitochondrial DNA (mtDNA) instability, NAD + depletion, Complex I inhibition, redox imbalance, and disrupted calcium homeostasis. We also summarize mitochondria-targeted interventions investigated in PD.