Significance of Mitochondrial Dysfunction in the Pathogenesis of Parkinson's Disease

Abstract

Parkinson’s disease (PD) is characterized by the degeneration of the dopaminergic neurons of the corpus striatum, which can be caused by the disruption of processes of mitochondrial homeostasis, including mitophagy, mitochondrial fusion and division, mitochondrial transport, accumulation of reactive oxygen species (ROS), and calcium signaling. Dopaminergic neurons are particularly vulnerable to mitochondrial dysfunction due to their polarized and expanded structure and high bioenergy needs. The molecular basis of these disorders is manifested in mutations of mitochondrial homeostasis proteins. Understanding the functions of these proteins and the disorders caused by these mutations can be used to create therapeutics for the treatment of PD and diagnostic biomarkers of PD. A comprehensive analysis of research papers to identify promising therapeutic targets and drug compounds that target them, as well as biomarkers of mitochondrial dysfunction that can be used in clinical practice for the treatment of PD has been conducted in the current review. This practical approach advantageously emphasizes the difference between this work and other reviews on similar topics. The selection of articles in this review was carried out using the following keyword searches in scientific databases: PubMed, Google Scholar, NSBI, and Cochrane. Next, the most relevant and promising studies were re-selected.

Keywords

• parkinson's disease
• neuron
• mitochondria
• mitochondrial dysfunction