There is a dual rationale to evaluate the expression levels of those genes: i) the role of LXRs and Abca1 in promoting memory formation and cognitive performance is now firmly established at least in animal models for Alzheimer's disease (review in [32]); ii) in an in vitro model it was demonstrated that expression level of LXR and some of their target genes is significantly inhibited by arsenic [33]. The gene discussed is ABCA1; the disease is early-onset autosomal dominant Alzheimer disease.