Oxidative stress in Alzheimer's disease.
Oxidative stress in Alzheimer's disease.
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DOI：
10.1016/j.pathophys.2006.05.004
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发表时间：
2006-08-01
期刊：
影响因子：
--
通讯作者：
Chauhan, Abha
中科院分区：
文献类型：
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作者：
Chauhan, Ved;Chauhan, Abha
氧化损伤是阿尔茨海默病（AD）病理生理学的主要特征。在这篇综述中，我们讨论了自由基介导的损害的生化成分参与的病理和临床症状的AD。我们解释了淀粉样β蛋白（Abeta），微管相关蛋白tau，早老素，载脂蛋白E，线粒体和蛋白酶如何在增加AD的氧化应激中发挥作用。Abeta不仅可以诱导氧化应激，而且其生成也由于氧化应激而增加。最后，提出了一个假设的模型，将氧化应激与β-淀粉样蛋白和AD中的神经元缠结病理联系起来。
Oxidative damage is a major feature in the pathophysiology of Alzheimer's disease (AD). In this review, we discuss free radical-mediated damage to the biochemical components involved in the pathology and clinical symptoms of AD. We explain how amyloid beta-protein (Abeta), microtubule-associated protein tau, presenilins, apolipoprotein E, mitochondria and proteases play a role in increasing oxidative stress in AD. Abeta not only can induce oxidative stress, but its generation is also increased as a result of oxidative stress. Finally, a hypothetical model linking oxidative stress with beta-amyloid and neurofibrillary tangle pathology in AD is proposed.