Modification: APOE: Knock-In
Disease Relevance: Alzheimer's Disease
Strain Name: B6.129P2-Apoetm2(APOE*3)Mae N8
Genetic Background: 129 x C57BL/6; back-crossed to C57BL/6
Availability: Taconic: Stock# 1548-F and 1548-M
Gene targeting was used to replace the endogenouse murine APOE gene with the human APOE3 allele. On a standard diet, homozygous mice have normal cholesterol and triglyceride levels, but are more susceptible than wild-type animals to diet-induced atherosclerosis (Sullivan et al., 1997); however, they are not as vulnerable as mice with APOE4 Targeted Replacement (Knouff et al., 1999).
Targeted replacement of the endogenous mouse APOE gene with the human APOE3 allele. Targeting vector contained exons 2-4 of human APOE3.
When visualized, these models will distributed over a 18 month timeline demarcated at the following intervals: 1mo, 3mo, 6mo, 9mo, 12mo, 15mo, 18mo+.
- Neuronal Loss
- Synaptic Loss
- Changes in LTP/LTD
- Cognitive Impairment
Changes in LTP/LTD
Research Models Citations
- Sullivan PM, Mezdour H, Aratani Y, Knouff C, Najib J, Reddick RL, Quarfordt SH, Maeda N. Targeted replacement of the mouse apolipoprotein E gene with the common human APOE3 allele enhances diet-induced hypercholesterolemia and atherosclerosis. J Biol Chem. 1997 Jul 18;272(29):17972-80. PubMed.
- Knouff C, Hinsdale ME, Mezdour H, Altenburg MK, Watanabe M, Quarfordt SH, Sullivan PM, Maeda N. Apo E structure determines VLDL clearance and atherosclerosis risk in mice. J Clin Invest. 1999 Jun;103(11):1579-86. PubMed.
No Available Further Reading