Previous studies have used genetic (ABCA1 overexpression) and pharmacologic (LXR or RXR agonists) approaches to show that increased lipidation of apoE lowers amyloid deposition and improves cognitive function in various AD mouse models, whereas decreased apoE lipidation in the absence of ABCA1 exacerbates amyloid pathology [30–33]. Here, ABCA1 is linked to Alzheimer disease.