Proteomic Complexity in Parkinson's Disease: A Redox Signaling Perspective of the Pathophysiology and Progression

Parkinson's disease (PD) is a prevalent age-related neurodegenerative disorder that results in the progressive impairment of motor and cognitive functions. The majority of PD cases are sporadic, and only 5% of patients are associated with mutations in a few genes, which cause the early onset or familial PD. Environmental toxic substances and the individual genetic susceptibility play a role in sporadic cases, but despite significant efforts to treat and prevent the disease, the pathophysiological mechanisms leading to its onset and progress are not fully understood. In the last decade, genomic and proteomic studies have shown an increasing molecular complexity of sporadic PD, suggesting that a broad spectrum of biochemical pathways underlie its progression. Recent investigations and the literature review suggest the potential role of deregulation of the sensitive-cysteine proteome as a convergent pathogenic mechanism that may contribute to this complexity, opening new therapeutic opportunities. (C) 2020 IBRO. Published by Elsevier Ltd. All rights reserved.

Automated summary

Parkinson's disease is a prevalent age-related neurodegenerative disorder, with the majority of cases being sporadic, though a small percentage are associated with gene mutations. Environmental toxic substances and individual genetic susceptibility play a role in the onset of the disease. Despite efforts to treat and prevent Parkinson's disease, the pathophysiological mechanisms leading to its onset and progression are not fully understood.