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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Age-related learning deficits in transgenic mice expressing the 751-amino acid isoform of human beta-amyloid precursor protein.
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Age-related learning deficits in transgenic mice expressing the 751-amino acid isoform of human beta-amyloid precursor protein.

机译：表达人类β-淀粉样蛋白前体蛋白的751个氨基酸同工型的转基因小鼠中与年龄有关的学习缺陷。

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摘要

The beta-amyloid precursor protein (beta-APP), from which the beta-A4 peptide is derived, is considered to be central to the pathogenesis of Alzheimer disease (AD). Transgenic mice expressing the 751-amino acid isoform of human beta-APP (beta-APP751) have been shown to develop early AD-like histopathology with diffuse deposits of beta-A4 and aberrant tau protein expression in the brain, particularly in the hippocampus, cortex, and amygdala. We now report that beta-APP751 transgenic mice exhibit age-dependent deficits in spatial learning in a water-maze task and in spontaneous alternation in a Y maze. These deficits were mild or absent in 6-month-old transgenic mice but were severe in 12-month-old transgenic mice compared to age-matched wild-type control mice. No other behavioral abnormalities were observed. These mice therefore model the progressive learning and memory impairment that is a cardinal feature of AD. These results provide evidence for a relationship between abnormal expression of beta-APP and cognitive impairments.
机译：衍生出β-A4肽的β-淀粉样蛋白前体蛋白（β-APP）被认为是阿尔茨海默病（AD）发病机理的核心。已证明，表达人类β-APP（751-APP751）751个氨基酸同工型的转基因小鼠会发展成早期AD样的组织病理学，其在大脑（尤其是在海马体）中会散布β-A4的沉积物和异常的tau蛋白表达，皮质和杏仁核。我们现在报告，β-APP751转基因小鼠在水迷宫任务和Y迷宫中的自发交替中在空间学习中表现出年龄依赖性的缺陷。与年龄匹配的野生型对照小鼠相比，这些缺陷在6个月大的转基因小鼠中轻微或不存在，但在12个月大的转基因小鼠中则严重。没有观察到其他行为异常。因此，这些小鼠模拟了进行性学习和记忆障碍，这是AD的主要特征。这些结果为β-APP异常表达与认知障碍之间的关系提供了证据。

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