The activation of LXRs has several biological consequences: (1) In cultured glial cells, it attenuates the inflammatory response induced by fibrillary Aβ, (2) In AD mouse models, it induces not only overexpression of the LXR-targets ABCA1, ABCG1, and APOE, but also reduces cognitive defects and improves brain pathology [100,101]. This evidence concerns the gene APOE and Alzheimer disease.