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降低β-淀粉样蛋白水平可挽救唐氏综合征小鼠模型的学习和记忆能力。

Lowering beta-amyloid levels rescues learning and memory in a Down syndrome mouse model.

机构信息

Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, New York, USA.

出版信息

PLoS One. 2010 Jun 3;5(6):e10943. doi: 10.1371/journal.pone.0010943.

Abstract

beta-amyloid levels are elevated in Down syndrome (DS) patients throughout life and are believed to cause Alzheimer's disease (AD) in adult members of this population. However, it is not known if beta-amyloid contributes to intellectual disability in younger individuals. We used a gamma-secretase inhibitor to lower beta-amyloid levels in young mice that model DS. This treatment corrected learning deficits characteristic of these mice, suggesting that beta-amyloid-lowering therapies might improve cognitive function in young DS patients.

摘要

β-淀粉样蛋白水平在唐氏综合征(DS)患者一生中都升高,并且被认为会导致该人群中成年人的阿尔茨海默病(AD)。然而,目前尚不清楚β-淀粉样蛋白是否会导致年轻个体的智力障碍。我们使用γ-分泌酶抑制剂来降低患有 DS 模型的年轻小鼠的β-淀粉样蛋白水平。这种治疗纠正了这些小鼠的学习缺陷,表明降低β-淀粉样蛋白的治疗方法可能会改善年轻 DS 患者的认知功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d37/2880593/3f8adb00e589/pone.0010943.g001.jpg

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