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)
<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

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