imilarly, in the CNS, ABCA1 interacts with lipid-poor/free ApoE to form HDL that is structurally distinct from ApoA-I-HDL (128), and it is recognised that HDL formed by different ApoE isoforms (ε2, ε3 and ε4) have different roles in the CNS, which has been particularly evident in studies related to Alzheimer’s disease (129). This evidence concerns the gene APOE and early-onset autosomal dominant Alzheimer disease.