Mitochondrial Dysfunction: A Precision Therapeutic Target in Parkinson’s Disease

Parkinson’s Disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra and the accumulation of the α-synuclein aggregates. Among the proposed pathogenic mechanisms, mitochondrial dysfunction plays a central role, contributing to bioenergetic failure, oxidative stress, and neuronal death. This article explores the mechanisms of mitochondrial impairment in PD, with a focus on genetic factors (PINK1, Parkin, LRRK2), mitophagy failure, and oxidative damage. Furthermore, it highlights current and emerging precision therapeutic strategies targeting mitochondrial health, including antioxidants, mitophagy inducers, and gene therapies. Targeting mitochondrial pathways presents a promising direction for disease modification and neuroprotection in Parkinson’s Disease.