Individuals carrying the ApoE-ε4 alleles, one of the ApoE isoforms, have a greater risk of developing AD because these alleles directly interact with Aβ and promote Aβ aggregation and plaque formation.26, 27In the AD mouse model overexpressing J20-human APP (hAPP), ABCA1 deficiency was shown to cause reduced lipid flux and a dramatic decrease in brain ApoE levels. This evidence concerns the gene ABCA1 and Alzheimer disease.