Title:An Insight into the Molecular Mechanism of Mitochondrial
Toxicant-induced Neuronal Apoptosis in Parkinson’s Disease
Volume: 23
Issue: 1
关键词:
细胞凋亡，电子传递链，环境污染物，线粒体，神经变性，帕金森病。
摘要: Parkinson’s disease (PD) is one of the most common progressive
neurodegenerative disorders affecting approximately 1% of the world’s population at the
age of 50 and above. Majority of PD cases are sporadic and show symptoms after the
age of 60 and above. At that time, most of the dopaminergic neurons in the region of
substantia nigra pars compacta have been degenerated. Although in past decades,
discoveries of genetic mutations linked to PD have significantly impacted our current
understanding of the pathogenesis of this devastating disorder, it is likely that the
environment also plays a critical role in the etiology of sporadic PD. Recent
epidemiological and experimental studies indicate that exposure to environmental
agents, including a number of agricultural and industrial chemicals, may contribute to the
pathogenesis of several neurodegenerative disorders, including PD. Furthermore, there
is a strong correlation between mitochondrial dysfunction and several forms of
neurodegenerative disorders, including Alzheimer’s disease (AD), Huntington’s disease
(HD), Amyotrophic lateral sclerosis (ALS) and PD. Interestingly, substantia nigra of
patients with PD has been shown to have a mild deficiency in mitochondrial respiratory
electron transport chain NADH dehydrogenase (Complex I) activity. This review
discusses the role of mitochondrial toxicants in the selective degeneration of
dopaminergic neurons targeting the electron transport system that leads to
Parkinsonism.
