While CSF derived from ABCG1−/− mice has increased levels of amyloid β (Aβ)(1-42) compared to wild-type mice [51], overexpressing ABCG1 did not alter the levels of Aβ, plaques, apoE levels, cholesterol efflux, or cognitive performance in mouse models of AD [52]. This evidence concerns the gene APOE and Alzheimer disease.