摘要
活性氧在细胞信号中起着生理作用,在疾病中也有一种病理作用,当抗氧化防御系统不堪重负时,造成氧化应激。然而,在这篇综述中,我们将重点放在还原应激,它可能被定义为一个病理生理的情况下,细胞变得比正常的、休息的状态的细胞更缩减。这可能发生在缺氧也可能是多种小但使氧化效应持续生成的疾病,导致抗氧化酶的激效超表达以至于细胞的隔间减少。这是阿尔茨海默氏症的病例。在阿尔茨海默氏症的高风险人群(因为他们携带ApoE4等位基因)遭受还原应激早在疾病的发生之前,甚至在轻度认知损害的发生之前。还原应激也可以是阿尔茨海默氏病的动物模型中发现(APP/PS1转基因小鼠),当其氧化还原状态是在年轻的时候确定的,比如,在本病发病之前。在后来的生活中,研究者们发展了氧化应激。在任何阿尔茨海默氏症的任何迹象或症状发生之前,了解还原性应激的发生有理论和实践的重要性,因为它可能是一个非常早期的疾病标志。
关键词: 自由基,抗氧化剂,神经退行性疾病,NADH/NAD+比值,氧化还原,生物标志物。
Current Alzheimer Research
Title:Reductive Stress: A New Concept in Alzheimer’s Disease
Volume: 13 Issue: 2
Author(s): A. Lloret, T. Fuchsberger, E. Giraldo and J. Vina
Affiliation:
关键词: 自由基,抗氧化剂,神经退行性疾病,NADH/NAD+比值,氧化还原,生物标志物。
摘要: Reactive oxygen species play a physiological role in cell signaling and also a pathological role in diseases, when antioxidant defenses are overwhelmed causing oxidative stress. However, in this review we will focus on reductive stress that may be defined as a pathophysiological situation in which the cell becomes more reduced than in the normal, resting state. This may occur in hypoxia and also in several diseases in which a small but persistent generation of oxidants results in a hormetic overexpression of antioxidant enzymes that leads to a reduction in cell compartments. This is the case of Alzheimer’s disease. Individuals at high risk of Alzheimer’s (because they carry the ApoE4 allele) suffer reductive stress long before the onset of the disease and even before the occurrence of mild cognitive impairment. Reductive stress can also be found in animal models of Alzheimer’s disease (APP/PS1 transgenic mice), when their redox state is determined at a young age, i.e. before the onset of the disease. Later in their lives they develop oxidative stress. The importance of understanding the occurrence of reductive stress before any signs or symptoms of Alzheimer’s has theoretical and also practical importance as it may be a very early marker of the disease.
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Cite this article as:
A. Lloret, T. Fuchsberger, E. Giraldo and J. Vina , Reductive Stress: A New Concept in Alzheimer’s Disease, Current Alzheimer Research 2016; 13 (2) . https://dx.doi.org/10.2174/1567205012666150921101430
DOI https://dx.doi.org/10.2174/1567205012666150921101430 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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