In the early 1990s, high cholesterol was found to be associated with the presence of ApoE4 alleles in clinically diagnosed Alzheimer's disease (Czech et al., 1994). In particular, high levels of LDL cholesterol resulted in a higher risk of dementia and stroke and the question posed was whether the administration of statins could diminish the incidence of these conditions (Moroney et al., 1999). The influential epidemiologic study of Wolozin and collaborators (Wolozin, Kellman, Ruosseau, Celesia, & Siegel, 2000) demonstrated that the patients taking the cholesterol-lowering drugs, which act as inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase, better known as statins, show a 60-73% lower prevalence of probable AD. These findings were followed by numerous studies regarding the impact of high cholesterol in creating favorable conditions for the generation of Ap peptides and further clinical investigations on the impact of statins (Sjogren & Blennow, 2005; Wolozin, 2004). This issue has been reassessed in this book in the closing chapter by Benjamin Wolozin in the context of interpreting AD clinical trials.
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