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锌快速诱导阿尔茨海默病β淀粉样蛋白形成。

Rapid induction of Alzheimer A beta amyloid formation by zinc.

作者信息

Bush A I, Pettingell W H, Multhaup G, d Paradis M, Vonsattel J P, Gusella J F, Beyreuther K, Masters C L, Tanzi R E

机构信息

Laboratory of Genetics and Aging, Massachusetts General Hospital, Boston.

出版信息

Science. 1994 Sep 2;265(5177):1464-7. doi: 10.1126/science.8073293.

Abstract

A beta 1-40, a major component of Alzheimer's disease cerebral amyloid, is present in the cerebrospinal fluid and remains relatively soluble at high concentrations (less than or equal to 3.7 mM). Thus, physiological factors which induce A beta amyloid formation could provide clues to the pathogenesis of the disease. It has been shown that human A beta specifically and saturably binds zinc. Here, concentrations of zinc above 300 nM rapidly destabilized human A beta 1-40 solutions, inducing tinctorial amyloid formation. However, rat A beta 1-40 binds zinc less avidly and is immune to these effects, perhaps explaining the scarcity with which these animals form cerebral A beta amyloid. These data suggest a role for cerebral zinc metabolism in the neuropathogenesis of Alzheimer's disease.

摘要

β淀粉样蛋白1-40是阿尔茨海默病脑淀粉样蛋白的主要成分,存在于脑脊液中,在高浓度(小于或等于3.7 mM)时仍相对可溶。因此,诱导β淀粉样蛋白形成的生理因素可能为该疾病的发病机制提供线索。研究表明,人β淀粉样蛋白能特异性且饱和地结合锌。在此,锌浓度高于300 nM时会迅速破坏人β淀粉样蛋白1-40溶液的稳定性,诱导形成具有染色特性的淀粉样蛋白。然而,大鼠β淀粉样蛋白1-40与锌的结合不那么紧密,且不受这些影响,这或许可以解释这些动物脑内β淀粉样蛋白形成较少的原因。这些数据表明脑锌代谢在阿尔茨海默病的神经发病机制中起作用。

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