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神经退行性变中致病机制之间的相互作用:氧化应激在肌萎缩侧索硬化症中的作用

Cross-talk between pathogenic mechanisms in neurodegeneration: the role of oxidative stress in Amyotrophic Lateral Sclerosis.

作者信息

Chico Lucia, Modena Martina, Lo Gerfo Annalisa, Ricci Giulia, Caldarazzo Ienco Elena, Ryskalin Larisa, Fornai Francesco, Siciliano Gabriele

机构信息

Department of Clinical and Experimental Medicine, University of Pisa, Via Savi 10, 56126 Pisa, Italy - Email:

出版信息

Arch Ital Biol. 2017 Dec 1;155(4):131-141. doi: 10.12871/00039829201744.

Abstract

The mechanisms underlying motoneuron degeneration in amyotrophic lateral sclerosis (ALS), a neurodegenerative disorder that affects the motor system with progressive paralysis, are complex and not yet fully understood. It is generally agreed that ALS is a multifactorial and multisystem disease due not only possibly to genetic causes but also to other factors like oxidative stress, mitochondrial dysfunction, protein aggregation, RNA dysmetabolism, autophagy, and excitotoxicity glutamate-mediate. Altered oxidative stress biomarker profile has been repeatedly reported in ALS patients, which may suggest that abnormal free radical production is relevant in the ALS pathogenesis. This review aims to investigate how oxidative stress can affect other proposed mechanisms of neurodegeneration in ALS.

摘要

肌萎缩侧索硬化症(ALS)是一种影响运动系统并导致进行性瘫痪的神经退行性疾病,其运动神经元变性的潜在机制复杂,尚未完全明确。人们普遍认为,ALS是一种多因素、多系统疾病,这不仅可能是由遗传因素引起的,还可能与其他因素有关,如氧化应激、线粒体功能障碍、蛋白质聚集、RNA代谢异常、自噬以及谷氨酸介导的兴奋性毒性。ALS患者中反复出现氧化应激生物标志物谱改变的情况,这可能表明异常的自由基产生与ALS发病机制相关。这篇综述旨在研究氧化应激如何影响ALS中其他提出的神经退行性变机制。

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