Research Models
Selected Results
1 Models
Name | Other Names | Strain Name | Genetic Background | Gene | Mutation | Modification Info | Modification | Disease | Neuropathology | Behavior/Cognition | Other Phenotype | Availability | Primary Paper | Visualization | |
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Mouse Models (1) |
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APOE4/Trem2*R47H, APOE*4/Trem2*R47H, APOE4.Trem2*R47H, LOAD1 | B6(SJL)-Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J | C57BL/6J | APOE, Trem2 | TREM2 R47H, APOE C130R (ApoE4) | This double-mutant line was generated by crossing APOE4 KI mice (Jackson Lab Stock# 027894), which carry a humanized APOE4 gene, to Trem2 R47H KI mice (Jackson Lab Stock # 027918), which have an R47H missense mutation knocked into the mouse Trem2 gene. | APOE: Knock-In; Trem2: Knock-In | Alzheimer's Disease | No neuron loss, amyloid plaques, neurofibrillary tangles, vascular leakage, myelin loss, or reactive microglia in mice up to 24 months of age. | Age-related changes in locomotor activity, motor coordination, and working memory, but no genotype-dependent differences through 24 months of age, compared with wild-type mice. | Age-, sex-, and region-dependent differences in glucose uptake and cerebral blood flow, compared with wild-type mice. Increased mortality at 24 months of age. Down-regulation of genes related to immune function and degradation of biological material in aged mice. | The Jackson Lab:Stock# 028709; Live | Kotredes et al., 2021 | Yes |
1 Visualizations
AD-related Research Models
Phenotypes Examined
- Plaques
- Tangles
- Neuronal Loss
- Gliosis
- Synaptic Loss
- Changes in LTP/LTD
- Cognitive Impairment
When visualized, these phenotypes will distributed over a 18 month timeline demarcated at the following intervals: 3mo, 6mo, 9mo, 1yr, 15mo, 18mo+.
Trem2 R47H KI x APOE4
Observed
Absent
-
Plaques at
Not observed in cortex or hippocampus up to 24 months of age.
-
Tangles at
Not observed in cortex or hippocampus up to 24 months of age.
-
Neuronal Loss at
Not observed in cortex or hippocampus up to 24 months of age.
-
Gliosis at
Microgliosis not observed in cortex or hippocampus up to 24 months of age.
-
Cognitive Impairment at
Age-related changes in locomotor activity, motor coordination, and working memory, but no genotype-dependent differences through 24 months of age, compared with wild-type mice.
No Data
-
Synaptic Loss at
No data.
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Changes in LTP/LTD at
No data.
Genes | Mutations | Modification | Disease | Neuropathology | Behavior/Cognition |
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APOE, Trem2 | TREM2 R47H, APOE C130R (ApoE4) | APOE: Knock-In; Trem2: Knock-In | Alzheimer's Disease | No neuron loss, amyloid plaques, neurofibrillary tangles, vascular leakage, myelin loss, or reactive microglia in mice up to 24 months of age. |
Age-related changes in locomotor activity, motor coordination, and working memory, but no genotype-dependent differences through 24 months of age, compared with wild-type mice. |