In animal models, mimicking the neurodegenerative disorder Alzheimer’s disease (AD), stimulating LXR/ABCA1 axis with agonists (T0901317 or GW3965), or increasing Abca1 expression alleviates the disorder, while deleting Abca1 expression aggravates the β-amyloid burden which is characteristic of AD (44, 45, 46). Here, ABCA1 is linked to Alzheimer disease.