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
Mouse Models (1)
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.

  • Changes in LTP/LTD at

    No data.

Genes Mutations Modification Disease Neuropathology Behavior/Cognition
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.

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