APP/PS1 Tg (B6;C3-Tg(APPswe,PSEN1dE9))
APP/PS1 Tg (B6;C3-Tg(APPswe,PSEN1dE9) mice) refers to a genetically engineered mouse model. Specifically:
* **APP:** Stands for Amyloid Precursor Protein.
* **PS1:** Stands for Presenilin 1.
* **Tg:** Stands for Transgenic. This means the mice have had foreign genes introduced into their genome.
* **B6;C3:** Refers to the genetic background strain of the mouse, a cross between C57BL/6 (B6) and C3H strains.
* **Tg(APPswe,PSEN1dE9):** This part indicates the specific transgenes introduced.
* **APPswe:** A mutation in the APP gene (specifically the Swedish mutation).
* **PSEN1dE9:** A mutation in the PSEN1 gene (specifically the exon 9 deletion mutation).
These mutations in APP and PSEN1 are commonly associated with familial Alzheimer's disease in humans. Therefore, these Tg mice are widely used as an animal model to study the mechanisms of Alzheimer's disease and to test potential therapies.
APP/PS1 Tg (B6;C3-Tg(APPswe,PSEN1dE9)) is,Transgenic mouse models widely used in Alzheimer's disease researchThese cells are genetically engineered to co-express human mutant APP (Swedish mutation) and PSEN1 (exon 9 deletion mutation) in neurons, and they form amyloid-beta deposits (plaques) in the brain with aging. The creation of these models is established by microinjecting DNA constructs containing these mutant genes into fertilized eggs, and then selecting and breeding lines that possess the transgene from the born offspring.
The main subjects of research utilization
| Disease under investigation | Hi, I came to find out the information about the seminar.
How to use the model |
| Alzheimer's disease |
Evaluation of amyloid-beta (Aβ) accumulation and aggregation (observation of senile plaque formation, quantification of Aβ40/42). Used for pathological analysis based on the amyloid cascade hypothesis and as a model for familial Alzheimer's disease (FAD). Evaluation of memory and learning abilities through cognitive function tests (Morris water maze, novel object recognition test, Y-maze test). |
| Cerebral amyloid angiopathy (CAA) |
Histological evaluation of Aβ deposition in blood vessel walls. Analysis of cerebrovascular disorder progression and pathological changes. Elucidation of vascular-related pathology through observation of neuroinflammation (microglial and astrocyte activation). |
| Mild cognitive impairment (MCI) |
Behavioral tests (novel object recognition test, Y-maze test) were conducted to assess early cognitive decline. Early neurodegenerative processes were elucidated using synaptic plasticity analysis (LTP measurement) and spine density evaluation. |
APP/PS1 Tg (B6;C3-Tg(APPswe,PSEN1dE9)) Review
Mutant presenilins specifically elevate the levels of the 42-residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific $\gamma$-secretase (Human Molecular Genetics, 13(2):159–170, 2004)
This paper (Jankowsky et al., 2004)A study that investigated the role of presenilin mutations in the pathogenesis of Alzheimer's disease in vivoAPP is cleaved by BACE1 and gamma-secretase to produce Aβ40 and Aβ42, and it is known that familial AD-related PS1 mutations increase the proportion of Aβ42. In this study, we analyzed transgenic mice co-expressing the APP Swedish mutation and a PS1 mutation, and showed that Aβ42 specifically increases while maintaining Aβ40, and furthermore, that Aβ42 concentration correlates with the rate of amyloid deposition. These results suggest that mutated presenilin may alter the specificity of gamma-secretase.
Reference: MAYO CLINIC (https://mayoclinic.elsevierpure.com/en/publications/mutant-presenilins-specifically-elevate-the-levels-of-the-42-resi/)
APP/PS1 Tg (B6;C3-Tg(APPswe,PSEN1dE9)) main products
B6;C3-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax (APP/PS1)
Transgenic mice co-expressing human APP Swedish mutant and PSEN1 deletion mutant form amyloid-beta plaques in the brain with aging. They are widely used as a model to reproduce the pathology of familial Alzheimer's disease and are suitable for analyzing neurodegeneration and cognitive decline. (Surveyed on May 18, 2026)
| Manufacturer/Distributor | The Jackson Laboratory |
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| Analysis items | Amyloid-beta accumulation, plaque formation, gene expression analysis, behavioral tests (learning and memory) |
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| Primary Endpoint | Aβ40/42 levels, amyloid deposition, cognitive decline, neuroinflammation, synaptic function changes |
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Reference: The Jackson Laboratory (https://www.jax.org/strain/004462)
B6J;C3H-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax (MMRRC #34829)
Transgenic mice co-expressing humanized APP Swedish mutant and PSEN1 deletion mutant in neurons. They produce human-type Aβ and form amyloid deposits in the brain at approximately 6-7 months of age. Widely used as a model for Alzheimer's disease pathology to analyze neurodegeneration and Aβ metabolism. (Surveyed May 18, 2026)
| Manufacturer/Distributor | Mutant Mouse Resource and Research Centers (MMRRC) |
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| Analysis items | Amyloid-beta production and accumulation, APP/PS1 expression analysis, immunoblotting, PCR, brain metabolism analysis |
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| Primary Endpoint | Abeta deposition, plaque formation timing (around 6-7 months of age), human Abeta detection, neuropathological changes |
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Reference: MMRRC (https://www.mmrrc.org/catalog/sds.php?mmrrc_id=34829)
Summary
APP/PS1 Tg (B6;C3-Tg(APPswe,PSEN1dE9)) models co-express human mutant APP and PSEN1, reproducing age-dependent amyloid-beta accumulation and cognitive decline. These models, available from The Jackson Laboratory and Mutant Mouse Resource and Research Centers, are widely used in Alzheimer's disease research.
In non-clinical studies, selecting a reliable disease model appropriate for the purpose is important. The following pages provide a list of disease models used in non-clinical studies. Please use this as a reference.
List of pathological models used in non-clinical studies
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