Presenilin‐2 Mutation Causes Early Amyloid Accumulation and Memory Impairment in a Transgenic Mouse Model of Alzheimer′s Disease

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Abstract
In order to clarify the pathophysiological role of presenilin‐2 (PS2) carrying the Volga German Kindred mutation (N141I) in a conventional mouse model of Alzheimer′s disease (AD) expressing amyloid precursor protein (APP) with the Swedish mutation (Tg2576 line), we generated a double transgenic mouse (PS2Tg2576) by crossbreeding the PS2 mutant with Tg2576 mice. Here, we demonstrate that the PS2 mutation induced the early deposition of amyloid β‐protein (Aβ) at 2‐3 months of age and progressive accumulation at 4‐5 months of age in the brains of the mutant mice. The PS2 mutation also accelerated learning and memory impairment associated with Aβ accumulation at 4‐5 months of age in Tg2576 mice. These results suggest that the PS2 mutation causes early cerebral amyloid accumulation and memory dysfunction. PS2Tg2576 mice are a suitable mouse model for studying amyloid‐lowering therapies.

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