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阿尔茨海默病大脑中经激光捕获显微切割的海马体1区锥体神经元中的β淀粉样肽水平。

Amyloid beta-peptide levels in laser capture microdissected cornu ammonis 1 pyramidal neurons of Alzheimer's brain.

作者信息

Aoki Mikio, Volkmann Inga, Tjernberg Lars O, Winblad Bengt, Bogdanovic Nenad

机构信息

Karolinska Institutet and Sumitomo Pharmaceuticals Alzheimer Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Novum plan 5, Huddinge, Sweden.

出版信息

Neuroreport. 2008 Jul 16;19(11):1085-9. doi: 10.1097/WNR.0b013e328302c858.

DOI:10.1097/WNR.0b013e328302c858
PMID:18596605
Abstract

Deposition of the amyloid beta-peptide (Abeta) is a pathophysiological event associated with Alzheimer's disease. Although much is known about the molecular composition of extracellular Abeta deposits, the role of the intracellular pool of Abeta is not fully understood. We investigated whether Abeta levels are increased in cornu ammonis 1 pyramidal neurons of Alzheimer's disease hippocampus, using laser capture microdissection to isolate the neurons and enzyme-linked immunosorbent assay for quantification. Our results showed increased Abeta42 levels and an elevated Abeta42/Abeta40 ratio in neurons from sporadic as well as from familial cases of Alzheimer's disease, whereas Abeta40 levels remain unchanged between the cases and controls. We speculate that intracellular accumulation of Abeta42 increase vulnerability of cornu ammonis 1 pyramidal neurons in Alzheimer's disease.

摘要

淀粉样β肽(Aβ)的沉积是与阿尔茨海默病相关的病理生理事件。尽管对细胞外Aβ沉积物的分子组成已了解很多,但细胞内Aβ池的作用尚未完全明了。我们利用激光捕获显微切割技术分离神经元,并采用酶联免疫吸附测定法进行定量,研究了阿尔茨海默病海马体中角回1区锥体神经元内的Aβ水平是否升高。我们的结果显示,散发性和家族性阿尔茨海默病病例的神经元中Aβ42水平升高,Aβ42/Aβ40比值升高,而病例组和对照组之间Aβ40水平保持不变。我们推测,Aβ42在细胞内的积累增加了阿尔茨海默病中角回1区锥体神经元的易损性。

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