Single App knock-in mouse models of Alzheimer's disease
T Saito, Y Matsuba, N Mihira, J Takano, P Nilsson… - Nature …, 2014 - nature.com
Nature neuroscience, 2014•nature.com
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.
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.
Abstract
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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