Abstract
3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, commonly referred to as statins, are widely used in the treatment of dyslipidaemia, in addition to providing primary and secondary prevention against cardiovascular disease and stroke. Statins’ effects on the central nervous system (CNS), particularly on cognition and neurological disorders such as stroke and multiple sclerosis, have received increasing attention in recent years, both within the scientific community and in the media. Current understanding of statins’ effects is limited by a lack of mechanism-based studies, as well as the assumption that all statins have the same pharmacological effect in the central nervous system. This review aims to provide an updated discussion on the molecular mechanisms contributing to statins’ possible effects on cognitive function, neurodegenerative disease, and various neurological disorders such as stroke, epilepsy, depression and CNS cancers. Additionally, the pharmacokinetic differences between statins and how these may result in statin-specific neurological effects are also discussed.
Highlights
3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, commonly referred to as statins, are widely used in the treatment of dyslipidaemia, in addition to providing primary and secondary prevention against cardiovascular disease and stroke
This study found that the protective effect of statin treatment was abolished following replenishment of FPP, but not GGPP
Whilst research into understanding statins’ central nervous system (CNS) effects has been extensive in recent years, there is still a distinct lack of mechanistic supportive evidence to justify the use of these compounds in the prevention or treatment of neurological disorders
Summary
3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, more commonly referred to as statins, are a class of cholesterol-lowering agents used for the treatment of dyslipidaemia and reduction of atherosclerotic cardiovascular disease risk. Their broad and potent effects on the lipid profile, in conjunction with cholesterol-independent (pleiotropic) cardioprotective effects, have resulted in statins being amongst the most highly prescribed medications worldwide. Unlike recent reviews and meta-analyses which explore the risks associated with statin use and the development of various neurological conditions (for these see [1,2,3,4]), this review focuses on the molecular mechanisms of statins in the CNS, how pharmacokinetic differences may influence statin action, and subsequent differences in effect between statin compounds
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