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Nat Neurosci. 2014 May;17(5):661-3. doi: 10.1038/nn.3697. Epub 2014 Apr 13.

Single App knock-in mouse models of Alzheimer's disease.

Author information

1
1] Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako-shi, Saitama, Japan. [2] Japan Science and Technology Agency, Saitama, Japan.
2
Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako-shi, Saitama, Japan.
3
Laboratory for Behavioral Genetics, RIKEN Brain Science Institute, Wako-shi, Saitama, Japan.
4
1] Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako-shi, Saitama, Japan. [2] Department of Molecular Medicinal Sciences, Division of Biotechnology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

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.

PMID:
24728269
DOI:
10.1038/nn.3697
[Indexed for MEDLINE]
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