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帕金森病中神经元死亡的原因。

Causes of neuronal death in Parkinson's disease.

作者信息

Schapira A H

机构信息

University Department of Clinical Neurosciences, Royal Free and University College Medical School, University College London, London, NW3 2PF, U.K.

出版信息

Adv Neurol. 2001;86:155-62.

Abstract

The etiology of PD is complex and may depend on multiple factors, both hereditary and environmental. A proportion of PD disease patients show a deficiency in mitochondrial respiratory chain function, in particular a defect of complex I, within neurons of the substantia nigra. Both mitochondrial mutations and toxic agents (endogenous and exogenous) have been demonstrated to cause a deficiency in complex I function. This is achieved by increasing the degree of, or susceptibility to, oxidative stress, which may contribute to apoptopic cell death. Future research directed toward developing neuroprotective strategies may reduce oxidative stress and stabilize or improve mitochondrial function.

摘要

帕金森病的病因复杂,可能取决于多种因素,包括遗传因素和环境因素。一部分帕金森病患者在黑质神经元中线粒体呼吸链功能存在缺陷,尤其是复合体I的缺陷。线粒体突变和有毒物质(内源性和外源性)均已被证明可导致复合体I功能缺陷。这是通过增加氧化应激的程度或易感性来实现的,而氧化应激可能导致细胞凋亡性死亡。针对开发神经保护策略的未来研究可能会减少氧化应激并稳定或改善线粒体功能。

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