Species: Mouse
Genes: Trem2
Modification: Trem2: Knock-In
Disease Relevance: Frontotemporal Dementia
Strain Name: C57BL/6J-Trem2em3Adiuj/J
Summary
Phenotype Characterization
When visualized, these models will distributed over a 18 month
timeline
demarcated at the following intervals: 1mo, 3mo, 6mo,
9mo, 12mo, 15mo, 18mo+.
Last Updated: 30 Nov 2018
Further Reading
No Available Further Reading
Species: Mouse
Genes: APOE, Trem2
Modification: APOE: Knock-In; Trem2: Knock-In
Disease Relevance: Alzheimer's Disease
Strain Name: B6(SJL)-Apoetm1.1(APOE*4)Adiuj Trem2em1Adiuj/J
Summary
Phenotype Characterization
When visualized, these models will distributed over a 18 month
timeline
demarcated at the following intervals: 1mo, 3mo, 6mo,
9mo, 12mo, 15mo, 18mo+.
Plaques
Not observed in cortex or hippocampus up to 24 months of age.
Tangles
Not observed in cortex or hippocampus up to 24 months of age.
Neuronal Loss
Not observed in cortex or hippocampus up to 24 months of age.
Gliosis
Microgliosis not observed in cortex or hippocampus up to 24 months of age.
Cognitive Impairment
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.
Last Updated: 04 Oct 2023
Further Reading
No Available Further Reading
Species: Mouse
Genes: Trem2
Modification: Trem2: Knock-Out
Disease Relevance: Alzheimer's Disease, Frontotemporal Dementia, Nasu-Hakola Disease
Strain Name: C57BL/6J-Trem2em2Adiuj/J
Summary
Phenotype Characterization
When visualized, these models will distributed over a 18 month
timeline
demarcated at the following intervals: 1mo, 3mo, 6mo,
9mo, 12mo, 15mo, 18mo+.
Last Updated: 04 Oct 2018
Further Reading
No Available Further Reading
Species: Mouse
Genes: Trem2
Modification: Trem2: Knock-In
Disease Relevance: Alzheimer's Disease
Strain Name: C57BL/6J-Trem2em1Adiuj/J
Summary
Phenotype Characterization
When visualized, these models will distributed over a 18 month
timeline
demarcated at the following intervals: 1mo, 3mo, 6mo,
9mo, 12mo, 15mo, 18mo+.
Plaques
Not observed in cortex or hippocampus up to 24 months of age.
Tangles
Not observed in cortex or hippocampus up to 24 months of age.
Neuronal Loss
Not observed in cortex or hippocampus up to 24 months of age.
Cognitive Impairment
Locomotor activity, motor coordination, and working memory similar to wild-type at 2 and 12 months of age.
Last Updated: 04 Oct 2023
Further Reading
No Available Further Reading
Species: Mouse
Genes: Trem2
Modification: Trem2: Knock-In
Disease Relevance: Frontotemporal Dementia
Strain Name: Trem2em1Bwef
Summary
Phenotype Characterization
When visualized, these models will distributed over a 18 month
timeline
demarcated at the following intervals: 1mo, 3mo, 6mo,
9mo, 12mo, 15mo, 18mo+.
Last Updated: 08 Mar 2018
Further Reading
No Available Further Reading
Species: Mouse
Genes: FUS
Mutations: FUSDelta14 truncation mutation
Modification: FUS: Knock-In
Disease Relevance: Amyotrophic Lateral Sclerosis
Strain Name: B6N;B6J-Fustm1Emcf/H
Summary
Phenotype Characterization
When visualized, these models will distributed over a 18 month
timeline
demarcated at the following intervals: 1mo, 3mo, 6mo,
9mo, 12mo, 15mo, 18mo+.
Lower Motor Neuron Loss
No lower motor neuron loss at 3 months but 14% reduction in the number of motor neurons in lumbar spinal cord at 12 months and 20% reduction by 18 months.
Cytoplasmic Inclusions
No increase in the number of spinal motor neurons that contain p62- or ubiquitin-positive inclusions in aged FUSDelta14 mice compared with aged wild-type mice.
NMJ Abnormalities
Reduction in the number of intact neuromuscular junctions (fully innervated endplates) in hindlimb lumbrical muscles by 18 months of age.
Motor Impairment
Normal motor activity at 3 months of age but impaired hindlimb function by 15 months.
Premature Death
Reduced survival starting at 19 months of age.
Last Updated: 01 Dec 2017
Further Reading
No Available Further Reading
Species: Mouse
Genes: APOE, APP, PSEN1
Modification: APOE: Knock-In; APP: Transgenic; PSEN1: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: N/A
The E4FAD, E3FAD, and E2FAD mouse models are crosses between the widely used 5xFAD mice (Tg6799 line) and the APOE4, APOE3, and APOE2 Targeted Replacement mice, respectively. These models were created to study the role of the three human isoforms of APOE on AD phenotypes. The mice described here were homozygous for the APOE allele and heterozygous of the 5xFAD mutations. In general, the EFAD mice display less severe phenotypes relative to the 5xFAD line.
Phenotype Characterization
When visualized, these models will distributed over a 18 month
timeline
demarcated at the following intervals: 1mo, 3mo, 6mo,
9mo, 12mo, 15mo, 18mo+.
Plaques
Plaques develop in the subiculum and deep cortical layers by 4 months.
Synaptic Loss
Protein levels of NMDA receptor subunits decreased from 2 to 6 months.
Gliosis
Microgliosis and astrocytosis in the subiculum and cortex at 6 months.
Cognitive Impairment
E2FAD mice had performance in learning and memory tasks comparable to E3FAD animals and better than E4FAD mice.
Last Updated: 09 Jun 2017
Further Reading
No Available Further Reading
Species: Mouse
Genes: APOE, APP, PSEN1
Modification: APOE: Knock-In; APP: Transgenic; PSEN1: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: N/A
The E4FAD, E3FAD, and E2FAD mouse models are crosses between the widely used 5xFAD mice (Tg6799 line) and the APOE4, APOE3, and APOE2 Targeted Replacement mice, respectively. These models were created to study the role of the three human isoforms of APOE on AD phenotypes. The mice described here were homozygous for the APOE allele and heterozygous of the 5xFAD mutations. In general, the EFAD mice display less severe phenotypes relative to the 5xFAD line.
Phenotype Characterization
When visualized, these models will distributed over a 18 month
timeline
demarcated at the following intervals: 1mo, 3mo, 6mo,
9mo, 12mo, 15mo, 18mo+.
Plaques
Plaques develop in the subiculum and deep cortical layers by 4 months.
Synaptic Loss
Protein levels of NMDA receptor subunits decreased from 2 to 6 months.
Gliosis
Microgliosis and astrocytosis in the subiculum and cortex at 6 months.
Cognitive Impairment
E3FAD mice had performance in learning and memory tasks comparable to E4FAD and E2FAD animals.
Last Updated: 09 Jun 2017
Further Reading
No Available Further Reading
Species: Mouse
Genes: APOE, APP, PSEN1
Modification: APOE: Knock-In; APP: Transgenic; PSEN1: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: N/A
The E4FAD, E3FAD, and E2FAD mouse models are crosses between the widely used 5xFAD mice (Tg6799 line) and the APOE4, APOE3, and APOE2 Targeted Replacement mice, respectively. These models were created to study the role of the three human isoforms of APOE on AD phenotypes. The mice described here were homozygous for the APOE allele and heterozygous of the 5xFAD mutations. In general, the EFAD mice display less severe phenotypes relative to the 5xFAD line.
Phenotype Characterization
When visualized, these models will distributed over a 18 month
timeline
demarcated at the following intervals: 1mo, 3mo, 6mo,
9mo, 12mo, 15mo, 18mo+.
Plaques
Plaques develop in the subiculum and deep cortical layers by 4 months.
Synaptic Loss
Decreased protein levels of PSD95 and NMDA receptor subunits by 4 months.
Gliosis
Microgliosis and astrocytosis in the subiculum and cortex at 6 months.
Cognitive Impairment
Modest learning deficits in the Morris water maze by 2 months. Progressive decrease in performance on learning and memory tasks.
Last Updated: 09 Jun 2017
Further Reading
No Available Further Reading
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