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人淀粉样β蛋白前体C末端片段的全身过表达导致转基因小鼠胰腺中阿尔茨海默β淀粉样纤维的积累。

Systemic overexpression of a C-terminal fragment of human amyloid beta-protein precursor causes accumulation of Alzheimer beta-amyloid fibrils in pancreas of transgenic mice.

作者信息

Shoji M, Kawarabayashi T, Sato M, Sasaki A, Matsubara E, Iizuka T, Harigaya Y, Hirai S

机构信息

Department of Neurology, Gunma University School of Medicine, Maebashi, Japan.

出版信息

Gerontology. 1996;42 Suppl 1:48-56. doi: 10.1159/000213824.

DOI:10.1159/000213824
PMID:8964522
Abstract

The deposition of amyloid beta-protein (A beta), derived from amyloid beta-protein precursor (beta APP), is a specific and early event in development of Alzheimer's disease. Transgenic mice carrying the carboxyl-terminus of beta APP gene linked to the cytomegalovirus enhancer/chicken beta-actin promoter sequence were studied. Deposition of amyloid fibrils, composing A beta, was observed in the transgenic pancreas, accompanied with cell degeneration. This result will provide a model to investigate the beta APP processing mechanism in vivo and a clue to generate possible A beta amyloidosis in animal brains.

摘要

源自淀粉样β蛋白前体(βAPP)的β淀粉样蛋白(Aβ)沉积是阿尔茨海默病发展过程中的一个特定早期事件。对携带与巨细胞病毒增强子/鸡β-肌动蛋白启动子序列相连的βAPP基因羧基末端的转基因小鼠进行了研究。在转基因小鼠的胰腺中观察到了由Aβ组成的淀粉样纤维沉积,并伴有细胞变性。这一结果将为体内研究βAPP加工机制提供一个模型,并为在动物大脑中引发可能的Aβ淀粉样变性提供线索。

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Systemic overexpression of a C-terminal fragment of human amyloid beta-protein precursor causes accumulation of Alzheimer beta-amyloid fibrils in pancreas of transgenic mice.人淀粉样β蛋白前体C末端片段的全身过表达导致转基因小鼠胰腺中阿尔茨海默β淀粉样纤维的积累。
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Accumulation of beta-amyloid fibrils in pancreas of transgenic mice.β-淀粉样纤维在转基因小鼠胰腺中的积累。
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