A pivotal role for cholesterol influence on production of the putative AD toxin, amyloid beta (Abeta), has been amply demonstrated. More importantly, this relationship has consistently been identified in both in vivo and in vitro studies. Lowering cholesterol levels has been shown to cause a beneficial effect on Abeta levels in animal models, and epidemiological data indicate a beneficial effect on the risk of AD with prior statin use. Blinded, placebo-controlled clinical investigations assessing the benefit of statins on cognitive indices in mild to moderate AD are ongoing and one will be reported on soon. A prospective study assessing the effect of statin use on the risk of AD is under way as an observational component of a placebo-controlled primary prevention trial testing anti-inflammatory agents. Nevertheless, the foregoing suggests that routine monitoring and intervention for elevated cholesterol levels among the elderly could promote more than a healthy heart.