神经炎症
转基因小鼠
淀粉样前体蛋白
表型
转基因
神经科学
淀粉样蛋白(真菌学)
基因剔除小鼠
突变
生物
基因敲除
阿尔茨海默病
疾病
细胞生物学
分子生物学
基因
基因敲除
医学
遗传学
病理
作者
Takashi Saito,Yukio Matsuba,Naomi Mihira,Jiro Takano,Per Nilsson,Shigeyoshi Itohara,Nobuhisa Iwata,Takaomi C. Saido
摘要
Experimental studies of Alzheimer's disease have largely depended on transgenic mice overexpressing amyloid precursor protein (APP). These mice, however, suffer from artificial phenotypes because, in addition to amyloid β peptide (Aβ), they overproduce other APP fragments. We generated knock-in mice that harbor Swedish and Beyreuther/Iberian mutations with and without the Arctic mutation in the APP gene. The mice showed typical Aβ pathology, neuroinflammation and memory impairment in an age-dependent manner.
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