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• W2046130135 abstract "Missense mutations in 2 homologous genes, presenilin 1 (PS1) and presenilin 2 (PS2), cause dementia in a subset of early-onset familial Alzheimer's disease (FAD) pedigrees. The purpose of the present study was to investigate whether PS2 mutation accelerates the onset of trace eyeblink conditioning deficits in an Alzheimer's disease (AD) mouse model overexpressing human amyloid precursor protein (APP) with the Swedish mutation (K670N, M671L) (Tg2576 mice). For this purpose, a double-transgenic mouse (PS2Tg2576 mice) was produced by cross-breeding transgenic mice carrying human mutant PS2 (N141I) with Tg2576 mice. Long-trace interval (trace interval=500ms) eyeblink conditioning was tested in the PS2Tg2576 mice at ages 3, 4, 6, and 12 months. At 3 months, PS2Tg2576 mice exhibited normal acquisition of conditioned responses (CRs) during trace eyeblink conditioning, whereas trace conditioning was significantly impaired in PS2Tg2576 mice at ages 4, 6, and 12 months. In contrast, Tg2576 mice showed intact memory performance during trace conditioning at 4 months. This cross-sectional study clearly indicates that PS2 mutation significantly accelerates the onset of cognitive impairment in associative trace eyeblink memory." @default.
• W2046130135 created "2016-06-24" @default.
• W2046130135 creator A5001666895 @default.
• W2046130135 creator A5053314310 @default.
• W2046130135 date "2013-03-01" @default.
• W2046130135 modified "2023-10-14" @default.
• W2046130135 title "Presenilin 2 mutation accelerates the onset of impairment in trace eyeblink conditioning in a mouse model of Alzheimer's disease overexpressing human mutant amyloid precursor protein" @default.
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• W2046130135 doi "https://doi.org/10.1016/j.neulet.2013.01.025" @default.
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