Several studies haveexplored the potential utility of LXRs agonistsin AD therapy.13,14,17,18In vivo studies using AD-liketransgenic mouse models have revealed that LXRs agonists provoke anupregulation of ApoE and ABCA1 expression, a marked reduction in Aβlevels, enhanced brain cholesterol turnover, and reversed contextualmemory deficits.19−21 However, a major concern with LXRs agonists is thatthey not only drive up transcription of ApoE and ABCA1 but also upregulategenes associated with fatty acid synthesis. This evidence concerns the gene ABCA1 and Alzheimer disease.