Parkinson’s Disease and Impairment in Mitochondrial Metabolism: A Pathognomic Signature

Abstract

Mitochondrial bioenergetics is vital for the proper functioning of cellular compartments. Impairments in mitochondrial DNA encoding the respiratory chain complexes and other assisting proteins, accumulation of intracellular reactive oxygen species, an imbalance in cellular calcium transport, or the presence of organic pollutants, high fat-ketogenic diets or toxins, and advancing age can result in complex disorders, including cancer, metabolic disease, and neurodegenerative disorders. Such manifestations are distinctly exhibited in several age-related neurodegenerative diseases, such as in Parkinson’s disease (PD). Defects in complex I along with perturbed signaling pathways is a common manifestation of PD. Impaired oxidative phosphorylation could increase the susceptibility to PD. Therefore, unraveling the mechanisms of mitochondrial complexes in clinical scenarios will assist in developing potential early biomarkers and standard tests for energy failure diagnosis and assist to pave a new path for targeted therapeutics against PD.