Early Phenotypic Changes in Transgenic Mice That Overexpress Different Mutants of Amyloid Precursor Protein in Brain
Open accessAbstract
Transgenic mice overexpressing different forms of amyloid precursor protein (APP), i.e. wild type or clinical mutants, displayed an essentially comparable early phenotype in terms of behavior, differential glutamatergic responses, deficits in maintenance of long term potentiation, and premature death. The cognitive impairment, demonstrated in F1 hybrids of the different APP transgenic lines, was significantly different from nontransgenic littermates as early as 3 months of age. Biochemical analysis of secreted and membrane-bound APP, C-terminal "stubs," and Abeta(40) and Abeta(42) peptides in brain indicated that no single intermediate can be responsible for the complex of phenotypic dysfunctions. As expected, the Abeta(42) levels were most prominent in APP/London transgenic mice and correlated directly with the formation of amyloid plaques in older mice of this line. Plaques were associated with immunoreactivity for hyperphosphorylated tau, eventually signaling some form of tau pathology. In conclusion, the different APP transgenic mouse lines studied display cognitive deficits and phenotypic traits early in life that dissociated in time from the formation of amyloid plaques and will be good models for both early and late neuropathological and clinical aspects of Alzheimer's disease.
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The spatial pattern of plaques in 5XFAD mice agreed well with those of previously reported Thy1 promoter-driven APP transgenic mice.
“As expected, the spatial pattern of plaques in 5XFAD mice agreed well with those of previously reported Thy1 promoter-driven APP transgenic mice (Sturchler-Pierrat et al., 1997; Moechars et al., 1999; Oddo et al., 2003).”
From Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation (2006) · cites this paper as Moechars et al., 1999
Transgenic mouse models successfully recapitulated Aβ plaque formation, increasing support for the amyloid hypothesis.
“These genetic findings led to several transgenic mouse models that successfully recapitulated Aβ plaque formation, increasing support for the hypothesis (Table 1) [23–29].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [27]
AD transgenic mice showed physiological and neuritic alterations prior to plaques.
“AD transgenic mice showed physiological [32, 74, 77, 124] and neuritic alterations [22, 125] prior to plaques”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [124]
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- Authors
- Moechars, D., Dewachter, I., Lorent, K., Reversé, D., Baekelandt, V., Naidu, A., Tesseur, I., Spittaels, K., Haute, C. V. D., Checler, F., Godaux, E., Cordell, B., & Van Leuven, F.
- Affiliations
- KU Leuven (BE)
- University of Mons (BE)
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1999-03
- Volume
- 274
- Issue
- 10
- Pages
- 6483-6492
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2169308121
- Cited by
- 668
- References
- 37
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 10 · 2023: 7 · 2022: 16 · 2021: 9 · 2020: 23 · 2019: 8 · 2018: 9 · 2017: 23 · 2016: 19 · 2015: 22 · 2014: 23 · 2013: 23 · 2012: 22
- FWCI
- 20.85
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- 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 transgenic mice, Alzheimer's disease, cognitive impairment, amyloid-beta 42, amyloid plaques, hyperphosphorylated tau, long-term potentiation
- MeSH terms
- Alzheimer Disease, Animals, Brain, Electrophysiology, Hippocampus, Mice, Transgenic, Mutation, Gene Expression, Amyloid beta-Protein Precursor, Mice
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