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阿尔茨海默病中淀粉样斑块部位连接蛋白43免疫反应性升高。

Elevated connexin43 immunoreactivity at sites of amyloid plaques in Alzheimer's disease.

作者信息

Nagy J I, Li W, Hertzberg E L, Marotta C A

机构信息

Department of Physiology, University of Manitoba, Winnipeg, Canada.

出版信息

Brain Res. 1996 Apr 22;717(1-2):173-8. doi: 10.1016/0006-8993(95)01526-4.

DOI:10.1016/0006-8993(95)01526-4
PMID:8738268
Abstract

The distribution of the astrocytic gap junctional protein, connexin43 (Cx43) was compared immunohistochemically with that of amyloid plaques in Alzheimer's Disease (AD) brain. By light microscopy, cortical areas containing numerous beta/A4 amyloid plaques exhibited increased immunostaining density for Cx43 and some plaques corresponded exactly to sites of intensified Cx43 immunoreactivity. By electron microscopy, Cx43 was localized to astrocytic gap junctions in AD brain. Increased Cx43 expression in AD may represent an attempt to maintain tissue homeostasis by augmented intercellular communication via gap junction formation between astrocytic processes that invest senile plaques, or alternatively, an aberrant induction of astrocytic Cx43 expression which may further compromise homeostasis and exacerbate pathological conditions in the microenvironment of amyloid plaques.

摘要

运用免疫组织化学方法,对阿尔茨海默病(AD)脑内星形胶质细胞缝隙连接蛋白连接蛋白43(Cx43)的分布与淀粉样斑块的分布进行了比较。通过光学显微镜观察,含有大量β/A4淀粉样斑块的皮质区域显示出Cx43免疫染色密度增加,并且一些斑块恰好对应于Cx43免疫反应性增强的部位。通过电子显微镜观察,Cx43定位于AD脑内的星形胶质细胞缝隙连接。AD中Cx43表达增加可能代表一种尝试,即通过围绕老年斑的星形胶质细胞突起之间形成缝隙连接来增强细胞间通讯,从而维持组织稳态;或者是星形胶质细胞Cx43表达的异常诱导,这可能会进一步破坏稳态并加剧淀粉样斑块微环境中的病理状况。

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