How Statins work for MS
Statins may inhibit progression of multiple sclerosis
CHAPEL HILL - Scientists from the University of North Carolina at Chapel Hill have established how statins -- cholesterol-lowering drugs -- inhibit inflammation and nerve cell damage caused by multiple sclerosis.
Preliminary research has shown that multiple sclerosis (MS) patients taking statins with their standard drug regimen develop less nerve cell damage over time than MS patients on standard therapy. Understanding the precise mechanisms by which statins fight multiple sclerosis is an important step toward approving the commonly used drugs for MS treatment, said Dr. Silva Markovic-Plese, associate professor of neurology, immunology and microbiology in the UNC School of Medicine.
In tests performed on blood samples from people with relapse-remitting MS, statins shut down several inflammatory processes. The statins inhibited the formation of immune-system cells called lymphocytes and monocytes, which cause inflammation by attacking the body's nerve cells.
"When we compared the effects of statins to well-understood MS therapies such as interferon, an anti-inflammatory, statins were equal if not stronger in some aspects," Markovic-Plese said. The researchers also examined blood samples from healthy people.
The study was published online July 25 in the Journal of Neuroimmunology and will appear in an upcoming print issue. The Myelin Project, a private research organization, funded part of the research.
Inflammation is the driving force behind MS, a disease in which immune cells attack the central nervous system at multiple sites. The attacks cause inflammation that damages the protective coating that insulates nerves and helps transmit nerve signals. The damage worsens as MS progresses, and patients lose the capability to control neurological functions such as vision, speech, and walking.
In the study, statins prevented inflammation by suppressing several genes that produce cytokines, secreted proteins that send messages regulating inflammation and the immune system. Statins also prevented the immune system from creating cells that damage nerve tissue.
"This study gives us a better understanding of what will happen when MS patients take statins," Markovic-Plese said. "Now we have some markers to follow in patients who take this medication, which will help us detect patients who respond to treatment."
The researchers predict that with further testing, statins may be used to enhance the current treatments for MS, which inhibit disease progression but don't completely stop it. Statins are already taken by millions of people to control cholesterol.
Markovic-Plese is leading a clinical trial at UNC comparing the standard therapy for MS (interferon beta-1a) combined with statin therapy or a placebo. The trial includes 30 patients and should be finished in one year.
"At the end of the trial we'll see how much benefit statins provide in addition to standard therapy," she said. The researchers will measure several cell markers identified in the current study.
Co-authors include Dr. Jianping Jin, Dr. Monica Montes, Danuta Sujkowski, Dr. Yunan Tang and Jennifer Smrtka, all of the UNC; Dr. Timothy Vollmer of the Barrow Neurological Institute at St. Joseph's Hospital and Medical Center, Phoenix, Ariz.; Dr. Shailendra Giri and Dr. Inderjit Singh of the Medical University of South Carolina in Charleston; and Xueyan Peng, of Yale University.
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