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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Age Factors
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Alzheimer Disease / genetics*
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Alzheimer Disease / metabolism
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Alzheimer Disease / physiopathology*
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Amyloid beta-Peptides / metabolism
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Amyloid beta-Protein Precursor / genetics*
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Analysis of Variance
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Animals
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Disease Models, Animal*
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Enzyme-Linked Immunosorbent Assay
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Gene Knock-In Techniques*
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Humans
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Maze Learning / physiology
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Mutation / genetics
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor