A number of studies have shown positive effects of statins in AD (Jick et al., 2000; Buxbaum et al., 2001 Buxbaum et al., , 2002 . This is in agreement with the previous studies demonstrating that depletion of cholesterol reduces Aβ in cultured neurons (Simons et al., 1998) . One recent study has suggested that fluvastatin is able to modify the trafficking of APP. Use of this drug was stated to increase lysosomal degradation of APP C-terminal fragments (CTFs) and hence facilitate Aβ clearance (Shinohara et al., 2010) . However, the reduction in Aβ levels is not necessarily linked with the cognitive benefits. A recent randomized, double-blinded, placebo-controlled trial of simvastatin showed reduced Aβ in treated patients, but no corresponding improvement in cognitive performance (ADAS-Cog score; Sano et al., 2011) . The biochemical studies are fairly uniform in that cholesterol depletion results in reductions in key ADrelated markers. However, the results of epidemiological research are unequivocal. The Cochrane Dementia and Cognitive Improvement Group study reported that statin treatment had no effect on the prevention or treatment of dementia (McGuinness et al., 2009a,b) . However, taking into account the highly variable relationship between the initiation of statin therapy and the time and severity of the AD, it is very difficult to get a conclusive assessment of the accumulated data on the beneficial effect of statins and any such study should use a defined set of criteria during epidemiological meta-analysis (Shepardson et al., 2011a,b) .