Cholesterol modulation as an emerging strategy for the treatment of Alzheimer's disease

The basis for therapeutic strategies targeting the amyloid-P protein (A bet a) has come from studies showing that accumulation and aggregation of the A beta within the brain is likely to cause Alzheimer's disease (A beta). Alo ng with an ever-increasing understanding of A beta metabolism, many potenti al therapeutic strategies aimed at altering A beta metabolism have emerged. Among the more intriguing targets for therapy are enzymes involved in chol esterol homeostasis, because it has been found that altering cholesterol ca n influence A beta metabolism in experimental model systems, and that chole sterol-lowering agents, specifically HMG-CoA reductase inhibitors, could re duce the incidence of A beta. It is likely that cholesterol influences A be ta metabolism in several ways, including altering A beta production and per haps altering A beta deposition and clearance. Thus, pharmacological modula tion of cholesterol levels could provide a relatively safe means to reduce A beta accumulation in the brain, and thereby prevent or slow the developme nt of A beta.