Genetic Modification of the Phenotypes Produced by Amyloid Precursor Protein Overexpression in Transgenic Mice
Abstract
Overexpression of Alzheimer amyloid precursor protein (APP) produces dramatically different phenotypes in transgenic mice depending on the genetic background. For example, concentrations of APP that produce amyloid plaques in outbred transgenic lines are lethal for inbred FVB/N or C57BL/6J mice. Expression of SOD1 transgenes is protective, suggesting involvement of oxidative damage in premature death, but ablation of Apoe had no significant effect. In contrast, FGF2 transgene overexpression enhances the lethal effects of APP. Differential survival does not appear to reflect genetic differences in APP processing, but rather host responses to APP or its derivatives.
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Overexpression of SOD1 in APP-overexpressing mice abolishes the lethal effects of the APP overexpression.
“overexpression of SOD1 in APP-overexpressing mice abolishes the lethal effects of the APP overexpression (40, 26).”
From Amyloid β oligomers constrict human capillaries in Alzheimer's disease via signaling to pericytes (2019) · cites this paper as [40]
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References 46 · Cited by 158
- Authors
- Carlson, G. A., Borchelt, D. R., Dake, A., Turner, S., Danielson, V., Coffin, J. D., Eckman, C., Meiners, J., Nilsen, S. P., Younkin, S. G., & Hsiao, K. K.
- Affiliations
- McLaughlin Research Institute (US)
- Johns Hopkins University (US)
- Brown University (US)
- Mayo Clinic (US)
- University of Minnesota (US)
- Corresponding author
- Carlson, G. A.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 1997-10-01
- Volume
- 6
- Issue
- 11
- Pages
- 1951-1959
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- OpenAlex
- W2101341993
- Cited by
- 158
- References
- 46
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 1 · 2020: 4 · 2019: 4 · 2018: 5 · 2017: 7 · 2016: 6 · 2015: 3 · 2014: 4 · 2013: 10 · 2012: 7
- FWCI
- 4.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Human Molecular Genetics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ag012685-04, 5r35ag007914-03, 5r01ag010681-05)
- National Institute on Aging (AG07914, AG10681, AG12685)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid precursor protein, APP overexpression, transgenic mice, genetic background, amyloid plaques, premature mortality, SOD1, oxidative damage, apolipoprotein E, FGF2, Alzheimer's disease
- MeSH terms
- Alleles, Animals, Apolipoproteins E, Genes, Lethal, Mice, Inbred C3H, Mice, Inbred C57BL, Mice, Transgenic, Phenotype, Protein Processing, Post-Translational, Superoxide Dismutase, Gene Expression, Fibroblast Growth Factor 2, Amyloid beta-Protein Precursor, Gene Deletion, Mice
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