Linking lipids, Alzheimer's and LXRs?

Abstract

Deposition of the β-amyloid (Aβ) peptide is thought to underlie development of Alzheimer's disease (AD). This pathological linkage has spurred considerable interest in therapeutic strategies to reduce Aβ production. It is becoming increasingly clear that altered cholesterol homeostasis can modulate Aβ production and/or accumulation. In this review, we discuss the molecular pathology of AD, the cholesterol connection and recent data suggesting that the oxysterol receptor, liver X receptor LXR (NR1H2 and NR1H3), may modulate these events.