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Abstract

Parkinson"s disease is the second most common progressive, age-linked neurodegenerative disorder. The sporadic form of the disease is usually idiopathic, where mitochondrial dysfunction is its major hallmark. Mitochondria are multifunctional dynamic organelles that carry out major cellular functions that get damaged by reactive oxygen species, deposition of lewy bodies, dopaminergic neuronal cell death, mitochondrial DNA mutations, and imbalance in fission/fusion that ultimately weakens mitophagy. In this review, the updated key roles and mechanisms of mitochondrial dysfunction structurally and functionally in the pathogenesis of sporadic Parkinson"s disease are discussed to understand the process of neurodegeneration. Research Data from numerous studies confirm mitochondrial dysfunction being the Basis of the disease. Here, we briefly bring the overview of illicit drug administration, oxidative stress, mitochondrial DNA mutations, mitochondrial genome mutations, alpha-synuclein aggregation, mitochondrial dynamics-fission and fusion, and the impairment of mitophagy in the disease pathogenesis. In conclusion, understanding mitochondrial dysfunction and its pathways can be a major target in treatment and prevention of Parkinson"s disease. INTRODUCTION:Parkinson"s disease (PD) was first started in an essay on "shaking palsy" by James Parkinson in 1817. In the beginning, it was discussed as "paralysis agitans" but Later was acknowledged as "maladie de Parkinson" or simply Parkinson"s disease by Charcot in 19 th century 1 . It has approximately 3-7% of lifetime risk after Alzheimer"s disease and is an age-linked progressive condition that is expected to increase exponentially in the elderly population.