Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease
Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease
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DOI：
10.1038/35050116
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发表时间：
2000-12-21
期刊：
影响因子：
64.8
通讯作者：
Arendash, GW
中科院分区：
文献类型：
--
作者：
Morgan, D;Diamond, DM;Arendash, GW
在阿尔茨海默病转基因小鼠模型中，用淀粉样β肽（AB）接种疫苗可显著减少淀粉样蛋白沉积（1）。为了确定疫苗接种是否具有有害或有益的功能后果，我们在阿尔茨海默病的不同转基因模型中测试了八个月的A β疫苗接种，其中小鼠随着淀粉样蛋白积累而出现学习缺陷（2，3）。在这里，我们表明，接种A β保护转基因小鼠的学习和年龄相关的记忆缺陷，通常发生在这种小鼠模型阿尔茨海默氏病。在测试疫苗的潜在有害作用时，所有小鼠在工作记忆的辐射臂水迷宫测试中表现出色。后来，在未处理的转基因小鼠表现出记忆缺陷的年龄，A β接种的转基因小鼠表现出上级于对照转基因小鼠的认知表现，并且最终表现得与非转基因小鼠一样好。在研究结束时，A β疫苗接种的小鼠的淀粉样蛋白负荷也有部分减少。因此，这种治疗方法可以预防并可能治疗阿尔茨海默氏痴呆症。
Vaccinations with amyloid-beta peptide (AB) can dramatically reduce amyloid deposition in a transgenic mouse model of Alzheimer's disease(1). To determine if the vaccinations had deleterious or beneficial functional consequences, we tested eight months of A beta vaccination in a different transgenic model for Alzheimer's disease in which mice develop learning deficits as amyloid accumulates(2,3). Here we show that vaccination with A beta protects transgenic mice from the learning and age-related memory deficits that normally occur in this mouse model for Alzheimer's disease. During testing for potential deleterious effects of the vaccine, all mice performed superbly on the radial-arm water-maze test of working memory. Later, at an age when untreated transgenic mice show memory deficits, the A beta -vaccinated transgenic mice showed cognitive performance superior to that of the control transgenic mice and, ultimately, performed as well as nontransgenic mice. The A beta -vaccinated mice also had a partial reduction in amyloid burden at the end of the study. This therapeutic approach may thus prevent and, possibly, treat Alzheimer's dementia.