评论“ApoE 靶向疗法快速清除β-淀粉样蛋白并逆转 AD 小鼠模型的缺陷”。
Comment on "ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models".
机构信息
Department of Environmental and Occupational Health, University of Pittsburgh, 100 Technology Drive, Pittsburgh, PA 15219, USA.
出版信息
Science. 2013 May 24;340(6135):924-c. doi: 10.1126/science.1235809.
Abstract
Cramer et al. (Reports, 23 March 2012, p. 1503; published online 9 February 2012) demonstrated in a mouse model for Alzheimer's disease (AD) that treatment of APP/PS1ΔE9 mice with bexarotene decreased Aβ pathology and ameliorated memory deficits. We confirm the reversal of memory deficits in APP/PS1ΔE9 mice expressing human APOE3 or APOE4 to the levels of their nontransgenic controls and the significant decrease of interstitial fluid Aβ, but not the effects on amyloid deposition.
摘要
克拉默等人（2012 年 3 月 23 日，第 1503 页；网上公布于 2012 年 2 月 9 日）在阿尔茨海默病（AD）的小鼠模型中证明，用贝沙罗汀治疗 APP/PS1ΔE9 小鼠可减少 Aβ 病理并改善记忆缺陷。我们证实了 APP/PS1ΔE9 小鼠中人类 APOE3 或 APOE4 的表达逆转了记忆缺陷，使其达到非转基因对照的水平，并且显著减少了脑间质液中的 Aβ，但对淀粉样蛋白沉积没有影响。
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