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Molecular pathophysiology of Parkinson's disease.
Annual Review of Neuroscience ( IF 12.1 ) Pub Date : 2005-07-19 , DOI: 10.1146/annurev.neuro.28.061604.135718
Darren J Moore 1 , Andrew B West , Valina L Dawson , Ted M Dawson
Affiliation  

Parkinson's disease (PD) is a progressive neurodegenerative movement disorder that results primarily from the death of dopaminergic neurons in the substantia nigra. Although the etiology of PD is incompletely understood, the recent discovery of genes associated with rare monogenic forms of the disease, together with earlier studies and new experimental animal models, has provided important and novel insight into the molecular pathways involved in disease pathogenesis. Increasing evidence indicates that deficits in mitochondrial function, oxidative and nitrosative stress, the accumulation of aberrant or misfolded proteins, and ubiquitin-proteasome system dysfunction may represent the principal molecular pathways or events that commonly underlie the pathogenesis of sporadic and familial forms of PD .

中文翻译:

帕金森氏病的分子病理生理学。

帕金森氏病(PD)是一种进行性神经退行性运动障碍,主要由黑质中的多巴胺能神经元死亡引起。尽管PD的病因学尚未完全理解,但最近发现的与罕见的单基因形式疾病相关的基因,以及更早的研究和新的实验动物模型,为涉及疾病发病机理的分子途径提供了重要且新颖的见解。越来越多的证据表明,线粒体功能的缺陷,氧化和亚硝化应激,异常或错误折叠的蛋白质的积累以及泛素-蛋白酶体系统功能障碍可能代表了主要的分子途径或事件,这些分子途径或事件通常是PD散发性和家族性形式的发病机制的基础。
更新日期:2019-11-01
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