Oxidative stress in Alzheimer disease
Oxidative stress in Alzheimer disease
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DOI：
10.4161/cam.3.1.7402
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发表时间：
2009-01-01
影响因子：
3.2
通讯作者：
Durany, Nuria
中科院分区：
文献类型：
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作者：
Gella, Alejandro;Durany, Nuria
阿尔茨海默病(AD)是一种进行性痴呆，影响着相当大比例的老龄人口。阿尔茨海默病的组织病理学改变包括神经细胞死亡、淀粉样斑块形成和神经原纤维缠结。也有证据表明，阿尔茨海默病患者的脑组织在疾病过程中暴露于氧化应激(如蛋白质氧化、脂肪氧化、DNA氧化和糖氧化)。晚期糖基化终末产物(AGEs)存在于AD的淀粉样斑块中，其胞外蓄积可能是糖化蛋白加速氧化所致。AGEs参与神经元死亡，导致直接(化学)和间接(细胞)自由基的产生，从而增加氧化应激。治疗阿尔茨海默病的药物的开发打破了氧化应激和神经退化的恶性循环，提供了新的机会。这些方法包括AGE抑制剂、抗氧化剂和抗炎物质，它们可以防止自由基的产生。
Alzheimer disease (AD) is a progressive dementia affecting a large proportion of the aging population. The histopathological changes in AD include neuronal cell death, formation of amyloid plaques and neurofibrillary tangles. There is also evidence that brain tissue in patients with AD is exposed to oxidative stress (e.g., protein oxidation, lipid oxidation, DNA oxidation and glycoxidation) during the course of the disease. Advanced glycation endproducts (AGEs) are present in amyloid plaques in AD, and its extracellular accumulation may be caused by an accelerated oxidation of glycated proteins. AGEs participate in neuronal death causing direct (chemical) and indirect (cellular) free radical production and consequently increase oxidative stress. The development of drugs for the treatment of AD that breaks the vicious cycles of oxidative stress and neurodegeneration offer new opportunities. These approaches include AGE-inhibitors, antioxidants and anti-inflammatory substances, which prevent free radical production.