Commonly referred to as APOE3 x APP/PS1 | Also known as: APO3xARTE10, APOE3xAPP-PS1, APOE3xAPP/PSEN1, APOE3xAPP-PSEN1, Model 22975
APOE3 x APP/PS1 (ARTE10) Alzheimer's Mouse Model
The APOE3xARTE10 mouse model combines Taconic’s APP/PS1 (ARTE10) amyloid-beta pathology framework with human APOE3 targeted replacement genetics. This model provides a common human APOE reference context for genotype-informed Alzheimer’s disease studies focused on amyloid pathology, plaque-associated glial response, and comparative APOE biology.
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| Model No. | Nomenclature | Genotype |
|---|---|---|
| 22975-M | B6.Cg-Apoetm2(APOE3)Mae Tg(Thy1-PSEN1M146V,-APP*Swe)10Arte | HOMxHOM |
| 22975-F | B6.Cg-Apoetm2(APOE3)Mae Tg(Thy1-PSEN1M146V,-APP*Swe)10Arte | HOMxHOM |
License fees are waived for custom breeding projects conducted at Taconic involving this model.
Combined Human APOE and APP/PS1 Amyloid Models for Alzheimer’s Drug Development
Evaluate amyloid-targeting therapies in human APOE3 and APOE4 genetic backgrounds using validated APOE replacement models combined with APP/PS1 (ARTE10) amyloid-beta alzheimer's disease model.
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Overview
Nomenclature: B6.Cg-Apoetm2(APOE3)Mae Tg(Thy1-PSEN1M146V,-APP*Swe)10Arte
The APOE3xARTE10 mouse model is designed for Alzheimer’s disease researchers who need to evaluate amyloid pathology in a defined human APOE3 context. By combining the APP/PS1 (ARTE10) amyloid-beta pathology model with human APOE3 targeted replacement genetics, 22975 enables study designs that compare common-reference human APOE biology against APOE4-associated biology and ARTE10 control contexts.
In the initial R&D characterization dataset, 22975 mice retained amyloid-beta plaques in key Alzheimer’s disease-relevant brain regions at approximately 11.5 months of age, while showing reduced plaque burden and reduced neuroinflammation relative to ARTE10 WT comparators in several regions and sex-stratified comparisons. This profile supports use of APOE3xARTE10 as a lower-pathology human APOE comparator within the paired APOE3/APOE4 ARTE10 model system.
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Recommended Controls
The recommended controls for this model are; C57BL/6NTac, APP/PS1 (ARTE10), and APOE3
Origin
This model was derived by crossing APOE3 (Model 1548) mice with APP/PS1 (ARTE10; Model 16347) mice, followed by successive crossbreeding to generate animals homozygous for both targeted alleles (HOM;HOM).
Genetics
Applications & Therapeutic Areas
- Neurobiology
- Alzheimer's Disease
- Amyloid Biology
- APOE Biology
- Neuroinflammation
- Model Selection
- Endpoint Strategy
Applications & Use Cases
- Reference comparator for APOE3 versus APOE4 amyloid studies in a share APP/PS1 (ARTE10) context.
- Evaluation of amyloid plaque burden and spatial distribution in human APOE3 background.
- Assessment of plaque-associated microglial and astrocytic responses in a genotype-defined amyloid model.
- Study-design comparator for amyloid-targeting interventions when APOE genotype could influence endpoint interpretation.
- Platform companion model for customers using APOE4xARTE10 to distinguish APOE4-associated findings from general human APOE effects.
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Data & Characterization
For 22975, the R&D report states that APOE3 decreased amyloid plaque density compared with ARTE10 WT controls in all brain regions except anterior cortex and thalamus. Male 22975 HOM animals showed decreased plaque density in all brain regions except thalamus, and 22975 HOM males had significantly less amyloid plaque density than female groups or WT males in anterior cortex, posterior cortex, and hippocampus. The conclusion also notes reduced neuroinflammation versus WT and E4, with 22975 males showing the lowest astrocyte activity among assessed strain/sex comparisons.
Figure 1. There is no difference between 22976-HOM (Arte10 x APOE4) and WT (Arte10) animals with regards to all brain regions measured EXCEPT the olfactory complex. There is a significant decrease in plaque density of 22975-HOM (Arte10 x APOE3) compared to WT (Arte10) in all brain regions EXCEPT the anterior cortex and thalamus. 22976-HOM had elevated plaques compared to 22975-HOM in the hippocampus. In summary, the presence of APOE4 does not change the amyloid plaque density in the brain of Arte10 mice except in the olfactory complex. The presence of APOE3 decreases the amyloid plaque density compared to those of Arte10 mice, except within the thalamus and anterior cortex. APOE4 has a significantly higher amyloid plaque density compared to APOE3 in the hippocampus. Two-way ANOVA *p<0.05.
Figure 2. There are sex-dependent differences with the level of amyloid plaque density. In the Arte10 x APOE4 (22976) both HOM and WT females (red and pink) had overall higher plaque levels than males (blue and teal) in the hippocampus and posterior cortex. Two-way ANOVA *p<0.05.
Figure 3. Sex differences were also present in the Arte10 x APOE3 (22975). Male HOM Arte10 x APOE3 (blue) animals had significantly less amyloid plaque density than females (WT or HOM) or WT males in the anterior and posterior cortex and the hippocampus. Two-way ANOVA *p<0.05
Figure 4. Given that there are sex differences in all three strains with regards to amyloid plaque density, we asked within a given sex whether there was a difference between strains. For females, there was a significant decrease in plaque density with the presence of APOE3 in the hippocampus and thalamus. A decrease was seen only in the olfactory complex with the presence of APOE4, otherwise plaques were equivalent to the WT (Arte10). Two-way ANOVA *p<0.05
Figure 5. For males, the presence of APOE3 decreased plaque density in all brain regions except the thalamus. The presence of APOE4 decreases plaque density in the posterior cortex and olfactory complex. Two-way ANOVA *p<0.05
Figure 6. Neuroinflammation = activated astrocyte and microglia density (# cells/area of tissue analyzed mm2)
22976 < WT for neuroinflammation; F > M
22975 << WT for neuroinflammation; F > M
There are sex-dependent differences in the level of neuroinflammation (microglia and astrocyte inflitration into the plaque and activation). Arte10 WT female animals (pink) have significantly more microglia then WT males and Arte10 x APOE4 (both sexes) within the amyloid plaque microenvironment in all brain regions except the thalamus and hippocampus.
Figure 7. For females, the presence of human APOE (blue and red) decreases the amount of microglia found within the amyloid beta plaque enviornment compared to WT controls (grey) regardless of the isoform in all brain regions except the thalamus. APOE3 (blue) had significantly less microglia than APOE4 (red) in all brain regions measured.
Figure 8. For males the findings are similar to females, the presence of human APOE (blue and red) decreases the amount of microglia found within the amyloid beta plaque environment compared to WT controls (grey) regardless of the isoform in all brain regions except the hippocampus and thalamus. APOE3 had significantly less microglia than APOE4 except the hippocampus and thalamus.
Figure 9. The are sex-dependent differences for the astrocyte component of neuroinflammation although to a lesser extent than with microglia. Only two brain regions (independent of strain) show sex differences for astrocyte inflitration of amyloid beta plaques, the anterior cortex and olfactory complex. The rest of the brain (hippocampus, posterior cortex, and thalamus) shows little to any difference in levels regardless of sex or the presence/absence of APOE4 an exception being the olfactory complex.
Figure 10. The are sex-dependent and strain differences for the astrocyte component of neuroinflammation as it applies to the presence/absence of APOE3. Male Arte10 x APOE3 animals have the lowest astrocyte inflitration into the amyloid beta plaque compared to all others in all brain regions except the hippocampus. The presence of the human APOE (regardless of isoform or sex) decreases the amount of astrocyte infiltration in the anterior and posterior cortex and olfactory complex compared to the WT (Arte10).
Figure 11. For females, the presence of the APOE3 isoform shows the lowest levels of astrocyte infiltration for the anterior and posterior cortex and the olfactory complex. APOE4 has equivalent levels to WT except within the anterior cortex and olfactory complex. There are no differences across the strains within the hippocampus or thalamus.
Figure 12. For males the findings are similar to females, the presence of the APOE3 isoform shows the lowest levels of astrocyte infiltration for the anterior and posterior cortex and the olfactory complex with the addition of the thalamus. Exactly as seen in females, APOE4 males have equivalent levels to WT except within the anterior cortex and olfactory complex. There are no differences across the strains within the hippocampus.
Conclusion: In summary, both the Arte10 x APOE4 and Arte10 x APOE3 show amyloid beta plaques in key brain regions at 11.5 months of age. Similar to the Arte10 (WT) there are sex differences in the severity of plaque phenotype and degree of neuroinflammation with females > males especially with regards to plaque density. The female Arte10 x APOE4 showed similar plaque burden to the wildtype Arte10 but less evidence of neuroinflammation (both within the plaque microenvironment and global). Male Arte10 x APOE4 had slightly decreased plaque burdens and less neuroinflammation compared to Arte10 (WT). With the presence of the E3 isoform, there was a decrease in plaque burden compared to Arte10 (WT) and E4 which was especially evident in the hippocampus. Neuroinflammation was also decreased compared to both models (E4 and WT) with Arte10 x APOE3 males showing the lowest astrocyte activity compared to all other strain/sex comparisons.
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APOE3 x APP/PS1 (ARTE10) Alzheimer's Mouse Model
Conditions of Use for Taconic Transgenic Models™
Taconic Transgenic Models™ (Models) are produced and distributed under rights to patents and intellectual property licensed from various institutions. Taconic sells the Models to purchasers, grants to each purchaser a right under Taconic's rights in such licensed patents and intellectual property to use the purchased Model in consideration of purchasers' acknowledgement of and agreement to the Terms and Conditions for Taconic Models, Products and Services and the following terms of use:
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Why Alzheimer’s Disease Models are Critical for Drug Discovery
Animal models are essential for understanding Alzheimer’s disease mechanisms, testing potential therapies, and bridging the gap between discovery and clinical success. Mouse models play a crucial role in replicating key features of AD, including β-amyloid accumulation, tau pathology, and neuroinflammation, allowing researchers to study disease progression and evaluate novel treatments. By providing a controlled, reproducible system to test drug efficacy and safety before human trials, these models help accelerate the development of effective therapeutics. Taconic Biosciences offers a diverse portfolio of Alzheimer’s disease mouse models, supporting researchers in their mission to combat this devastating disease.
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