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多巴胺能神经元因氧化应激而沉默:帕金森病死亡级联反应的早期步骤?

Dopaminergic neurons reduced to silence by oxidative stress: an early step in the death cascade in Parkinson's disease?

作者信息

Michel Patrick P, Ruberg Merle, Hirsch Etienne

机构信息

INSERM U679, Experimental Neurology and Therapeutics, 75013 Paris, France.

出版信息

Sci STKE. 2006 Apr 25;2006(332):pe19. doi: 10.1126/stke.3322006pe19.

Abstract

Parkinson's disease (PD) is a common neurodegenerative disorder that is most often sporadic, but in some cases it can be inherited as a simple Mendelian trait. The most important pathological feature of the disease is the death of brainstem dopaminergic neurons in the substantia nigra, which leads to characteristic motor symptoms. The etiology of PD remains unknown, but mitochondrial dysfunction and oxidative stress may contribute actively to the underlying pathomechanism. New studies suggest that K(ATP) channel activation may represent a downstream effector of these two cellular anomalies.

摘要

帕金森病(PD)是一种常见的神经退行性疾病,大多为散发性,但在某些情况下可作为一种简单的孟德尔性状遗传。该疾病最重要的病理特征是黑质中脑干细胞多巴胺能神经元的死亡,这会导致典型的运动症状。帕金森病的病因尚不清楚,但线粒体功能障碍和氧化应激可能在潜在的发病机制中起积极作用。新的研究表明,K(ATP)通道激活可能是这两种细胞异常的下游效应器。

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