Age-related cognitive decline and nesting behavior in an APPswe/PS1 bigenic model of Alzheimer's disease.
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.
Filali
Mohammed
M
Laboratory of Endocrinology and Genomics, CHUL Research Center (CHUQ) and Department of Anatomy and Physiology, Laval University, 2705 Laurier boul., Québec, Canada. Mohammed.Filali@crchul.ulaval.ca
Lalonde
Robert
R
D000375:Aging; D000544:Alzheimer Disease / Q000523:psychology*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D001362:Avoidance Learning; D003072:Cognition Disorders; D004193:Discrimination Learning; D004195:Disease Models, Animal; D006801:Humans; D007859:Learning Disabilities; D008297:Male; D018782:Maze Learning; D051379:Mice; D008822:Mice, Transgenic; D009154:Mutation; D009425:Nesting Behavior; D009483:Neuropsychological Tests; D053764:Presenilin-1 / Q000235:genetics; D058255:Protease Nexins; D011956:Receptors, Cell Surface / Q000235:genetics; D013997:Time Factors
C545487:APP protein, human; D016564:Amyloid beta-Protein Precursor; D053764:Presenilin-1; D058255:Protease Nexins; D011956:Receptors, Cell Surface