Because the ApoE-ε4 isoform of the protein is less efficient than ApoE-ε3 and ApoE-ε2 in transporting brain cholesterol [41], our findings could be interpreted as the result of a dysregulation in cholesterol homeostasis, which might contribute to the increased risk of AD observed in the ε4-homozygous group. This evidence concerns the gene APOE and Alzheimer disease.