Research Models
Selected Results
3 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 (3)
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<p>-</p>, <p>APOE2 Humanized Knock-in</p> | B6.129P2-Apoetm1(APOE*2)Mae N9 | 129 x C57BL/6; back-crossed to C57BL/6 | APOE | APOE R176C (ApoE2) | Targeted gene replacement of the endogenous murine APOE gene with the human APOE2 allele. Targeting construct included exons 2-4 of APOE2. | APOE: Knock-In | Alzheimer's Disease, Multiple Conditions | None reported. White-matter integrity, as assessed by fractional anisotropy, was reported to be higher in the hippocampus and caudate putamen of year-old female APOE2 mice, compared with APOE3 females; these genotype differences were not seen in males. | Findings are mixed, with some studies reporting that APOE genotype—in some cases, interacting with sex or age—affects performance in behavioral assays. | Characteristics of type III hyperlipoproteinemia. Plasma cholesterol and triglyceride levels 2-3x higher than APOE3 mice. Impaired clearance of very-low-density lipoprotein (VLDL) particles. Atherosclerotic plaques. Compared with APOE3 mice, APOE2 mice exhibited higher levels of glucose uptake in the cortex and hippocampus and up-regulation of genes involved in glucose utilization. | Taconic: Stock# 1547-F and 1547-M | Sullivan et al., 1998 | No | ||
<p>-</p>, <p>APOE3 Humanized Knock-in</p> | B6.129P2-Apoetm2(APOE*3)Mae N8 | 129 x C57BL/6; back-crossed to C57BL/6 | APOE | Targeted replacement of the endogenous mouse APOE gene with the human APOE3 allele. Targeting vector contained exons 2-4 of human APOE3. | APOE: Knock-In | Alzheimer's Disease, Multiple Conditions | None reported. APOE3 was considered the neutral allele against which the other human APOE genotypes were compared in most studies of neurological phenotypes in Targeted Replacement mice. Data comparing Targeted Replacement mice to wild-type mice are limited. | Findings are mixed, with some studies reporting that APOE genotype—in some cases, interacting with sex or age—affects performance in behavioral assays. | On a standard diet, homozygous mice have normal cholesterol and triglyceride levels, but are more susceptible than wild-type animals to diet-induced atherosclerosis. Data comparing neurological phenotypes in Targeted Replacement mice to wild-type mice are sparse, but APOE3 mice resemble wild-type mice with respect to aspects of hippocampal anatomy and physiology, including LTP and neurogenesis. | Taconic: Stock# 1548-F and 1548-M | Sullivan et al., 1997 | No | |||
<p>-</p>, <p>APOE4 Humanized Knock-in</p> | B6.129P2-Apoetm3(APOE*4)Mae N8 | 129 x C57BL/6, back-crossed to C57BL/6 | APOE | APOE C130R (ApoE4) | Targeted replacement of the endogenous murine APOE gene with the human APOE4 allele; targeting construct contained exons 2–4 of APOE4. | APOE: Knock-In | Alzheimer's Disease, Multiple Conditions | Mice do not develop amyloid plaques or neurofibrillary tangles. Genotype-dependent differences in brain structure have been reported, but findings are mixed. While some groups have found smaller hippocampal volumes, enlarged ventricles, and compromised white matter in APOE4 mice compared with APOE3, others did not observe these differences. | Findings are mixed, with some studies reporting that APOE genotype—in some cases, interacting with sex or age—affects performance in behavioral assays. | Increased risk of atherosclerosis. Elevated cholesterol, APOE, and APOB-48 on a high fat diet. Transcriptomic and functional evidence for increased aerobic glycolysis and decreased mitochondrial respiration in APOE4 compared with APOE3 mice. Electrophysiological and imaging studies suggest that aged APOE4 mice exhibit neural hyperactivity compared with APOE3 mice in some brain regions. | Taconic: Stock# 1549-F or 1549-M | Knouff et al., 1999 | No |