Oxidative stress, cell cycle, and neurodegeneration.
Oxidative stress, cell cycle, and neurodegeneration.
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DOI：
10.1172/jci18182
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发表时间：
2003-03
期刊：
影响因子：
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通讯作者：
J. A. Klein;S. Ackerman
中科院分区：
文献类型：
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作者：
J. A. Klein;S. Ackerman
虽然许多研究已经检查了在晚发型神经退行性疾病中是否存在增加的活性氧物种(ROS)，但神经元在氧化应激条件下死亡的机制在很大程度上仍不清楚。最近的证据表明，与终末分化神经元死亡有关的一种机制是异常重新进入细胞周期。在阿尔茨海默病(AD)患者(1例)、唐氏综合症患者(2例)和几种小鼠神经退行性模型(3-5例)中已经报道了这种现象。我们将讨论有关氧化应激对神经退行性变的影响以及氧化应激与非计划细胞周期重入之间的可能联系的最新发现，对这些发现的理解可能导致开发神经退行性疾病的治疗药物的新策略。
While numerous studies have examined the existence of increased reactive oxygen species (ROS) in later-onset neurodegenerative disorders, the mechanism by which neurons die under conditions of oxidative stress remains largely unknown. Fairly recent evidence has suggested that one mechanism linked to the death of terminally differentiated neurons is aberrant reentry into the cell cycle. This phenomenon has been reported in Alzheimer disease (AD) patients (1), Down syndrome patients (2), and several mouse neurodegenerative models (3–5). We will discuss recent findings regarding the influence of oxidative stress on neurodegeneration and possible connections between oxidative stress and unscheduled cell cycle reentry, the understanding of which could lead to new strategies in the development of therapeutic agents for neurodegenerative disorders.