Copper and Oxidative Stress in the Pathogenesis of Alzheimer's Disease
Copper and Oxidative Stress in the Pathogenesis of Alzheimer's Disease
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DOI：
10.1021/bi3006169
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发表时间：
2012-08-14
期刊：
影响因子：
2.9
通讯作者：
Axelsen, Paul H.
中科院分区：
文献类型：
--
作者：
Eskici, Goezde;Axelsen, Paul H.
铜是一种具有氧化还原活性的金属，具有许多重要的生物学作用。因此，其分布和氧化状态受到严格的监管。大量的临床病理学、环境和流行病学证据表明，铜的失调与阿尔茨海默病的发病机制密切相关。其他轻过渡金属，如铁和锌，可能会影响铜的调节，通过竞争铜的结合位点和转运。针对铜调节的治疗干预是有希望的，但我们对铜生物化学，淀粉样蛋白生成和大脑氧化应激性质的理解存在很大差距。
Copper is a redox-active metal with many important biological roles. Consequently, its distribution and oxidation state are subject to stringent regulation. A large body of clinicopathological, circumstantial, and epidemiological evidence suggests that the dysregulation of copper is intimately involved in the pathogenesis of Alzheimer's disease. Other light transition metals such as iron and zinc may affect copper regulation by competing for copper binding sites and transporters. Therapeutic interventions targeting the regulation of copper are promising, but large gaps in our understanding of copper biochemistry, amyloidogenesis, and the nature of oxidative stress in the brain must be addressed.