Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease

被引:1254
|
作者
Morgan, D [1 ]
Diamond, DM
Gottschall, PE
Ugen, KE
Dickey, C
Hardy, J
Duff, K
Jantzen, P
DiCarlo, G
Wilcock, D
Connor, K
Hatcher, J
Hope, C
Gordon, M
Arendash, GW
机构
[1] Univ S Florida, Dept Pharmacol, Alzheimer Res Lab, Tampa, FL 33612 USA
[2] Univ S Florida, Dept Psychol, Tampa, FL 33612 USA
[3] Univ S Florida, Dept Med Microbiol & Immunol, Tampa, FL 33612 USA
[4] Univ S Florida, Dept Biol, Alzheimer Res Lab, Tampa, FL 33612 USA
[5] James A Haley Vet Adm Med Ctr, Tampa, FL 33612 USA
[6] Mayo Clin Jacksonville, Dept Pharmacol, Jacksonville, FL 32224 USA
[7] Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA
关键词
D O I
10.1038/35050116
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:982 / 985
页数:5
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