Recent results implicating cholesterol metabolism in the pathophysiology of Alzheimer's disease (AD) bring cholesterol to the forefront of AD research. Research from genetics, epidemiology, and cell biology all converge, suggesting that cholesterol plays a central role in the biology of amyloid precursor protein and the toxic peptide generated by its cleavage, beta-amyloid (Abeta). The ability of cholesterol to modulate Abeta production suggests opportunities for therapeutic intervention, although the functional significance underlying the connection between cholesterol and Abeta remains to be investigated.