Filali Mohammed, Lalonde Robert
Laboratory of Endocrinology and Genomics, CHUL Research Center (CHUQ) and Department of Anatomy and Physiology, Laval University, 2705 Laurier boul., Québec, Canada.
Brain Res. 2009 Oct 6;1292:93-9. doi: 10.1016/j.brainres.2009.07.066. Epub 2009 Jul 28.
A large series of 3-, 6-, 9-, and 12-month-old bigenic mice (N=240) with Swedish APP and A246E PS1 mutations was investigated in nest-building, spontaneous alternation, and two learning tasks. Progressive cognitive impairment was observed in APPswe/PS1 mice relative to controls for nest-building, spontaneous alternation, the reversal phase of left-right discrimination learning in a water-filled T-maze, and in retention of passive avoidance learning. The behavioral deficits in transgenic mice start at 6 months, appearing to offer an opportunity for assessing potential therapeutic agents in attenuating or preventing Alzheimer's disease.
对大量携带瑞典APP和A246E PS1突变的3个月、6个月、9个月和12个月大的双基因小鼠(N = 240)进行了筑巢、自发交替以及两项学习任务的研究。相对于对照组,在APPswe/PS1小鼠中观察到渐进性认知障碍,涉及筑巢、自发交替、在充满水的T型迷宫中左右辨别学习的反转阶段以及被动回避学习的记忆保持。转基因小鼠的行为缺陷始于6个月,这似乎为评估减轻或预防阿尔茨海默病的潜在治疗药物提供了机会。