Mitochondria first became of interest to PD researchers after people exposed to the mitochondrial toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) developed Parkinsonism that responded to levodopa therapy.1 MPTP can enter the brain and is converted to a daughter compound MPP+, which selectively enters dopaminergic neurons and inhibits the normal bioenergetic functioning of mitochondria.1
Despite the key role that the mitochondria appears to play in the development of PD, as outlined on the slide, attempts to target mitochondrial dysfunction with novel therapeutics have yet to demonstrate clear efficacy.2 However, the possibility that patients with PD could be stratified based on their mitochondrial subtypes allows for the possibility of more personalized medicines, targeting the specific mitochondrial disruptions seen in PD.2