Lipids play an important part as risk factors for Alzheimer's disease. This article summarizes the current understanding of the molecular mechanism by which amyloid-beta (A beta) peptides regulate cholesterol and sphingomyelin metabolism, and how in return cholesterol and sphingomyelin regulate A beta pepticle production. An understanding of the physiological function of amyloid precursor protein processing and A beta function is critical for the development of future therapeutic approaches, e.g. statin treatment. Copyright (c) 2006 S. Karger AG, Basel.