Recent studies suggest that HMG-CoA reductase inhibitors or statins may be a treatment option for MS. These are popular drugs that are being used to treat high cholesterol in patients and that the effects of these drugs may be comparable to those of the beta-interferons for reducing autoimmune attack on the central nervous system. Because the drug has a favorable safety profile, the authors point out that it is difficult to carry out clinical trials to determine the efficacy of this treatment. They also point out that "overly optimistic reports" in popular media are complicating evaluation of the treatments.


[*] Neuhaus O, Stuve O, Zamvil SS and Hartung HP (2005). Evaluation of HMG-CoA Reductase Inhibitors for Multiple Sclerosis : Opportunities and Obstacles. CNS Drugs 19: 833-41. The disease-modifying agents currently used in the treatment of multiple sclerosis (MS) are not completely effective and are associated with adverse effects and high costs. Thus, alternative treatment options are highly desirable. HMG-CoA reductase inhibitors (statins), widely prescribed as cholesterol-lowering agents, may be a future treatment option for MS - either in an add-on therapy regimen or alone - as they have been shown to exhibit potent immunomodulatory effects. Several recent reports have demonstrated that HMG-CoA reductase inhibitors prevent and reverse chronic and relapsing experimental autoimmune encephalomyelitis, an animal model of MS. Furthermore, in vitro experiments with human immune cells have shown an immunomodulatory mode of action of HMG-CoA reductase inhibitors that is comparable to that of interferon-beta, an established treatment for MS. An open-label clinical trial assessing simvastatin treatment in patients with MS revealed a significant decrease in the number and volume of new lesions, as assessed using magnetic resonance imaging, and a favourable safety profile. A large multicentre, placebo-controlled phase II clinical trial assessing atorvastatin in patients with a clinically isolated syndrome (i.e. a single clinical event that is indicative of demyelination, and that predisposes to the development MS) has recently been initiated. However, prospective placebo-controlled trials of HMG-CoA reductase inhibitors in definite MS are difficult to perform because of ethical and financial issues. Furthermore, overly optimistic reports in the popular media, as well as the often uncontrolled access to HMG-CoA reductase inhibitors by patients with MS, complicate the evaluation of HMG-CoA reductase inhibitors as a realistic future treatment option for MS. Department of Neurology, Heinrich Heine University, Dusseldorf, Germany.