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表达阿尔茨海默病淀粉样前体蛋白的转基因小鼠。

Transgenic mice expressing Alzheimer amyloid precursor proteins.

作者信息

Hsiao K

机构信息

Department of Neurology, University of Minnesota, Minneapolis 55455, USA.

出版信息

Exp Gerontol. 1998 Nov-Dec;33(7-8):883-9. doi: 10.1016/s0531-5565(98)00045-x.

DOI:10.1016/s0531-5565(98)00045-x
PMID:9951631
Abstract

Nearly a decade after the identification of the Alzheimer amyloid precursor protein (APP) gene several groups of investigators have created transgenic mice expressing APP that simulate some of the prominent behavioral and pathological features of Alzheimer's disease (Quon et al., 1991; Games et al., 1995; Hsiao et al., 1995, 1996; Moechars et al., 1996; Sturchler-Pierrat et al., 1997). These features, which are present to various degrees in different lines of mice, include age-related impairment in learning and memory, neuronal loss, gliosis, neuritic changes, amyloid deposition, and abnormal tau phosphorylation. No mouse model exhibiting every neuropathological feature of Alzheimer's disease exists. Whether an exact simulation of Alzheimer neuropathology is required to understand neural dysfunction in Alzheimer's disease is unclear. Various mouse models of Alzheimer's disease are summarized in this article.

摘要

在确定阿尔茨海默病淀粉样前体蛋白(APP)基因近十年后,几组研究人员培育出了表达APP的转基因小鼠,这些小鼠模拟了阿尔茨海默病的一些突出行为和病理特征(Quon等人,1991年;Games等人,1995年;Hsiao等人,1995年、1996年;Moechars等人,1996年;Sturchler-Pierrat等人,1997年)。这些特征在不同品系的小鼠中程度各异,包括与年龄相关的学习和记忆障碍、神经元丢失、胶质细胞增生、神经突变化、淀粉样蛋白沉积以及异常的tau蛋白磷酸化。不存在表现出阿尔茨海默病所有神经病理学特征的小鼠模型。尚不清楚理解阿尔茨海默病中的神经功能障碍是否需要精确模拟阿尔茨海默病神经病理学。本文总结了各种阿尔茨海默病小鼠模型。

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Transgenic mice expressing Alzheimer amyloid precursor proteins.表达阿尔茨海默病淀粉样前体蛋白的转基因小鼠。
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Intraneuronal Abeta accumulation precedes plaque formation in beta-amyloid precursor protein and presenilin-1 double-transgenic mice.在β-淀粉样前体蛋白和早老素-1双转基因小鼠中,神经元内β-淀粉样蛋白(Aβ)的积累先于斑块形成。
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Cerebrolysin decreases amyloid-beta production by regulating amyloid protein precursor maturation in a transgenic model of Alzheimer's disease.在阿尔茨海默病转基因模型中,脑活素通过调节淀粉样蛋白前体成熟来减少β-淀粉样蛋白的产生。
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