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挑战传统观念:多巴胺氧化应激在帕金森病中的病因学作用。

Challenging conventional wisdom: the etiologic role of dopamine oxidative stress in Parkinson's disease.

作者信息

Ahlskog J Eric

机构信息

Department of Neurology, Mayo Clinic, Rochester, Minnesota 55905, USA.

出版信息

Mov Disord. 2005 Mar;20(3):271-82. doi: 10.1002/mds.20362.

DOI:10.1002/mds.20362
PMID:15580550
Abstract

Oxidative stress is well documented in Parkinson's disease (PD) and has been attributed to dopamine oxidative metabolism. However, evidence of oxidative stress is found in a variety of neurodegenerative disorders, suggesting that more general factors are responsible or that cytodestructive processes secondarily generate oxyradical products. Increasing evidence points away from dopamine metabolism as an important contributor to PD neurodegeneration. Predictions from the dopamine oxidative stress hypothesis of PD reveal multiple inconsistencies. Although the clinical and therapeutic importance of the nigrostriatal dopaminergic system is undeniable, PD neuropathology is much more widespread.

摘要

氧化应激在帕金森病(PD)中已有充分记载,且被认为与多巴胺的氧化代谢有关。然而,在多种神经退行性疾病中都发现了氧化应激的证据,这表明可能存在更普遍的因素,或者细胞破坏过程会继发产生氧自由基产物。越来越多的证据表明,多巴胺代谢并非PD神经退行性变的重要促成因素。PD多巴胺氧化应激假说的预测存在多处矛盾。尽管黑质纹状体多巴胺能系统的临床和治疗重要性不可否认,但PD神经病理学的影响范围要广泛得多。

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