Therefore, activation of the LXR pathway presents attractive potential as a therapeutic strategy in Alzheimer’s disease for enhancing P-gp activity, and alleviating the Aβ burden and its associated neurodegenerative effects [51,52], as well as in ischaemic strokes to help restore the BBB following hypoxia-induced BBB breakdown [47,53]. Here, PGP is linked to early-onset autosomal dominant Alzheimer disease.