There has been considerable interest in the association between cholesterol, its upstream isoprenoid family members (FPP and GGPP) and Alzheimers disease (AD).However, the HMG-CoA reductase inhibitors, statins, have had mixed effects in preventing or treating AD.One explanation for those disappointing results is that statins are targeting the wrong protein.We have recently found that FPP and GGPP levels and gene expression of FPP synthase and GGPP synthase were significantly elevated in brain tissue of Alzheimer disease patients as compared with normal neurological controls; cholesterol levels and HMG-CoA reductase gene expression were unchanged.FPP is a precursor of both cholesterol and GGPP.