One of the core pathological features of Parkinson’s disease (PD) is mitochondrial dysfunction in substantia nigra dopaminergic neurons, which is specifically manifested by decreased activity of mitochondrial respiratory chain complex I (NADH dehydrogenase), mitochondrial DNA (mtDNA) damage, excessive accumulation of reactive oxygen species (ROS), and ultimately neuronal apoptosis (41, 42). This evidence concerns the gene NDUFV1 and Parkinson disease.