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β-淀粉样蛋白增加PC12细胞的胆碱电导:阿尔茨海默病中毒性的可能机制。

beta-Amyloid increases choline conductance of PC12 cells: possible mechanism of toxicity in Alzheimer's disease.

作者信息

Galdzicki Z, Fukuyama R, Wadhwani K C, Rapoport S I, Ehrenstein G

机构信息

Laboratory of Neurosciences, National Institute on Aging, NIH, Bethesda, MD 20892.

出版信息

Brain Res. 1994 May 23;646(2):332-6. doi: 10.1016/0006-8993(94)90101-5.

Abstract

When beta-amyloid-(1-40) is added to PC12 cells, there is an increase in choline conductance that is proportional to the beta-amyloid concentration. If a similar effect occurs in cholinergic brain cells of Alzheimer's disease patients, the intracellular choline concentration would be reduced, leading to a decrease in the production of acetylcholine. This could explain the reduced level of acetylcholine that has been found in post-mortem brain tissue of Alzheimer's disease patients.

摘要

当将β-淀粉样蛋白(1-40)添加到PC12细胞中时,胆碱电导会增加,且与β-淀粉样蛋白浓度成正比。如果在阿尔茨海默病患者的胆碱能脑细胞中发生类似效应,细胞内胆碱浓度将会降低,导致乙酰胆碱生成减少。这可以解释在阿尔茨海默病患者的死后脑组织中发现的乙酰胆碱水平降低的现象。

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