Although it is not clear whether LXR activation can also prevent plaque formation, most recent data from the P. Tontonoz laboratory demonstrated that global deletion of LXRα or LXRβ in APP transgenic mice results in increased amyloid plaque load [27] which further strengthened the idea that LXR signalling and LXR responsive genes are important determinants of AD pathogenesis (at least deposition of fibrillar Aβ and its clearance) [14,21,27]. Here, NR1H3 is linked to Alzheimer disease.