Essential role of LXRs has been studied in APP/PS1 transgenic mouse model, where LXR activation decreased the amyloid burden and improved memory [44], [12] LXR activation has also been shown to suppress amyloid deposition and marked impairment of memory in APP23 mice induced by high fat diet [45] Activation of LXRs has further been demonstrated to produce anti-inflammatory actions [13] Treatment of AD mouse with LXR agonists documented to induce suppression of microglia activation and potent inhibition of cox2, mcp1 as well as iNos in glial cells hence exerting anti-inflammatory actions [46]. This evidence concerns the gene APP and Alzheimer disease.