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Chinese Journal of Neurology ; (12): 1025-1033, 2022.
Article in Chinese | WPRIM | ID: wpr-957999

ABSTRACT

Parkinson′s disease (PD) is a complex neurodegenerative disorder typically known for characteristic loss of dopaminergic neurons in the substantia nigra striatum. To date, therapeutic approaches for PD are still lacking due to the multifactorial etiology and complicated pathogenesis. Thus, the studies relative to the biological mechanisms and drug development of PD are the hotspot in this field. In recent years, numerous studies suggest that the PD is associated with mitochondrial dysfunction which is affected by multiple genes regulation. Genome-wide association studies have proved that monogenic PD gene locus is associated with mitochondrial dysfunction. Although there are many studies on how PD pathogenic genes regulate mitochondrial dysfunction then affect neuronal physiological function and ultimately lead to the PD, the effects of mutations in PD-associated genes on mitochondrial dysfunction remain not fully understood. In this review, the literature discussing the mechanisms of mitochondrial dysfunction in the context of PD was summarized with the aim to implicate the potential opportunities for therapeutically targeting mitochondria.

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