The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
Augmented Senile Plaque Load in Aged Female β-Amyloid Precursor Protein-Transgenic Mice
Open accessAbstract
Transgenic mice (Tg2576) overexpressing human beta-amyloid precursor protein with the Swedish mutation (APP695SWE) develop Alzheimer's disease-like amyloid beta protein (Abeta) deposits by 8 to 10 months of age. These mice show elevated levels of Abeta40 and Abeta42, as well as an age-related increase in diffuse and compact senile plaques in the brain. Senile plaque load was quantitated in the hippocampus and neocortex of 8- to 19-month-old male and female Tg2576 mice. In all mice, plaque burden increased markedly after the age of 12 months. At 15 and 19 months of age, senile plaque load was significantly greater in females than in males; in 91 mice studied at 15 months of age, the area occupied by plaques in female Tg2576 mice was nearly three times that of males. By enzyme-linked immunosorbent assay, female mice also had more Abeta40 and Abeta42 in the brain than did males, although this difference was less pronounced than the difference in histological plaque load. These data show that senescent female Tg2576 mice deposit more amyloid in the brain than do male mice, and may provide an animal model in which the influence of sex differences on cerebral amyloid pathology can be evaluated.
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“Also as it has been reported with other APP/PS1 transgenic mice, we observed a sex-specific effect on amyloid deposition with 5XFAD female mice developing amyloid deposits earlier compared to male littermates [27], [31], [32].”
From Lack of LDL receptor enhances amyloid deposition and decreases glial response in an Alzheimer's disease mouse model (2011) · cites this paper as [31]
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“A similar sex-specific amyloid deposition phenotype has been previously reported with other APP transgenic mouse models (Callahan et al., 2001; Wang et al., 2003).”
From Overexpression of Low-Density Lipoprotein Receptor in the Brain Markedly Inhibits Amyloid Deposition and Increases Extracellular Aβ Clearance (2009) · cites this paper as Callahan et al., 2001
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Cited by
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Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP
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Metadata
- Authors
- Callahan, M. J., Lipinski, W. J., Bian, F., Durham, R. A., Pack, A., & Walker, L. C.
- Affiliations
- Pfizer (United States) (US)
- Corresponding author
- Callahan, Michael J.
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2001-03
- Volume
- 158
- Issue
- 3
- Pages
- 1173-1177
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC1850367
- OpenAlex
- W2164192847
- Cited by
- 274
- References
- 30
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 8 · 2023: 5 · 2022: 8 · 2021: 14 · 2020: 10 · 2019: 14 · 2018: 9 · 2017: 10 · 2016: 9 · 2015: 17 · 2014: 15 · 2013: 16 · 2012: 10
- FWCI
- 7.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Pfizer
- Tulane University
- York University
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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 plaques, amyloid-beta, amyloid precursor protein, Tg2576 mice, sex differences, aging, Alzheimer's disease, amyloid deposition, hippocampus, neocortex, Aβ40, amyloid-beta 42
- MeSH terms
- Aging, Alzheimer Disease, Animals, Disease Models, Animal, Female, Hippocampus, Male, Mice, Transgenic, Peptide Fragments, Sex Factors, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Neocortex, Mice, Plaque, Amyloid
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