Fighting Parkinson's disease: The return of the mitochondria

Parkinson's disease (PD) is the most common neurodegenerative movement disorder, worldwide. PD neuroenergetically affects the extrapyramidal system, by the progressive loss of striatal dopaminergic neurons in the substantia nigra pars compacta, leading to motor impairment. During the progression of PD, there will be an increase in mitochondrial dysfunction, reactive oxygen species (ROS), stress and accumulation of alpha-synuclein in neurons. This results in mitochondrial mutations altering their function and fission-fusion mechanisms and central nervous system (CNS) degeneration. Intracellular mitochondrial dysfunction has been studied for a long time in PD due to the decline of mitochondrial dynamics inside neurons. Mitochondrial damage-associated molecular patterns (DAMPs) have been known to contribute to several CNS pathologies especially PD pathogenesis. New and exciting evidence regarding the exchange of mitochondria between healthy to damaged cells in the central nervous system (CNS) and the therapeutic use of the artificial mitochondrial transfer/transplant (AMT) marked a return of this organelle to develop innovative therapeutic procedures for PD. The focus of this review aims to shed light on the role of mitochondria, both intra and extracellularly in PD, and how AMT could be used to generate new potential therapies in the fight against PD. Moreover, we suggest that mitochondrial therapy could work as a preventative measure, motivating the field to move towards this goal.

Automated summary

Parkinson's disease is a common neurodegenerative movement disorder characterized by the loss of dopaminergic neurons in the brain. Mitochondrial dysfunction, oxidative stress, and accumulation of alpha-synuclein contribute to the progression of PD. Recent evidence suggests that mitochondrial transfer/transplantation could be a potential therapeutic approach for PD.