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.

帕金森氏病（PD）是一种普遍存在的年龄相关性神经退行性疾病，可导致运动和认知功能的逐步损害。大多数PD病例是散发性的，只有5％的患者与少数基因突变相关，这些基因会引起PD或家族性PD的早发。环境有毒物质和个体遗传易感性在偶发病例中起作用，但是尽管在治疗和预防该疾病方面做出了巨大努力，但导致其发病和进展的病理生理机制仍未得到充分理解。在过去的十年中，基因组和蛋白质组学研究表明，散发性PD的分子复杂性不断提高，这表明其进展是多种生化途径的基础。