摘要
背景:阿尔茨海默病(AD)是一种以认知功能进行性下降为特征的神经退行性疾病,是全球范围内的主要医疗保健挑战。越来越多的证据表明,线粒体功能障碍介导的氧化应激在AD的病理生理过程中起重要作用。因此,认为抗氧化酶的生理活化对增加的氧化应激反应是预防神经病理学的。其中一种内源性防御是NADPH醌氧化还原酶1(NQO1)。 NQO1是一种胞质二聚体黄素蛋白,催化醌和相关分子的双电子还原,旨在增加它们的溶解度和排泄。与其作为II期应激反应蛋白的作用一样,改变的NQO1表达与几种病理状态和病症(包括AD)相关。 结论:本综述总结了NQO1与AD病理学的关系。了解这种关联将提供进一步的洞察疾病的发病机制。更重要的是,最近对影响NQO1表达或其活性的药物的兴趣提供了希望这种方法可能导致治疗AD的新的治疗选择。
关键词: 阿尔茨海默病(AD),NADPH醌氧化还原酶1(NQO1),神经原纤维缠结(NFT),淀粉样β蛋白,线粒体功能障碍,神经退行性疾病。
Current Alzheimer Research
Title:Alzheimer's Disease and NQO1: Is there a Link?
Volume: 15 Issue: 1
关键词: 阿尔茨海默病(AD),NADPH醌氧化还原酶1(NQO1),神经原纤维缠结(NFT),淀粉样β蛋白,线粒体功能障碍,神经退行性疾病。
摘要: Background: Alzheimer's disease (AD) is a neurodegenerative disease characterised by a progressive decline in cognitive function and represents a major healthcare challenge worldwide. Increasing evidence indicates that mitochondrial dysfunction mediated oxidative stress plays a significant role in the pathophysiological process of AD. Therefore, the physiological activation of antioxidant enzymes that respond to increased oxidative stress is thought to prevent neuropathology. One of those endogenous defences is NADPH quinone oxidoreductase 1 (NQO1). NQO1 is a cytosolic homodimeric flavoprotein that catalyses the two-electron reduction of quinones and related molecules aimed at increasing their solubility and excretion. In line with its role as a phase II stress response protein, altered NQO1 expression is associated with several pathological conditions and disorders including AD.
Conclusion: This review summarizes the association between NQO1 and AD pathology. Understanding this association will provide further insight into the pathogenesis of the disease. More importantly, recent interest in drugs that affect NQO1 expression or its activity provides hope that this approach could lead to novel therapeutic options for the treatment of AD.
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Cite this article as:
Alzheimer's Disease and NQO1: Is there a Link?, Current Alzheimer Research 2018; 15 (1) . https://dx.doi.org/10.2174/1567205014666170203095802
DOI https://dx.doi.org/10.2174/1567205014666170203095802 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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