| Literature DB >> 24728269 |
Takashi Saito1, Yukio Matsuba2, Naomi Mihira2, Jiro Takano2, Per Nilsson2, Shigeyoshi Itohara3, Nobuhisa Iwata4, Takaomi C Saido2.
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.Entities:
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Year: 2014 PMID: 24728269 DOI: 10.1038/nn.3697
Source DB: PubMed Journal: Nat Neurosci ISSN: 1097-6256 Impact factor: 24.884