APOE and Cognitive impairment: Furthermore, ABCA1 reduction is considered one of the reasons why ApoE4-containing lipoproteins are poorly lipidated [69,70]; indeed, the treatment of different mouse models expressing ApoE4 with the ABCA1 agonist CS-6253 or the LXR agonist T0901317 have been shown to increase ApoE4 lipidation, as well as to reduce ApoE4-driven Aβ accumulation and cognitive deficits [71,72].