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铜与阿尔茨海默病发病机制中的氧化应激。

Copper and oxidative stress in the pathogenesis of Alzheimer's disease.

机构信息

Department of Pharmacology, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA 19104, USA.

出版信息

Biochemistry. 2012 Aug 14;51(32):6289-311. doi: 10.1021/bi3006169. Epub 2012 Jul 31.

DOI:10.1021/bi3006169
PMID:22708607
Abstract

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.

摘要

铜是一种具有许多重要生物学作用的氧化还原活性金属。因此,其分布和氧化态受到严格的调节。大量的临床病理、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,可能通过竞争铜结合位点和转运体来影响铜的调节。针对铜调节的治疗干预措施很有前景,但我们对铜生物化学、淀粉样蛋白形成以及大脑氧化应激性质的理解还存在很大差距。

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