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A New Discovery May Lead to Treatment of MS
A way to repair the damage to the sheathing of nerve cells that causes multiple sclerosis -- at least in mice -- has been discovered by three researchers at the University of California at Irvine.
Some day the discovery may lead to an effective treatment for the worst effects of the disease.
UCI biologists Thomas Lane, Michael Liu and Hans Keirstead infected a group of laboratory mice with a virus that made them begin to lose the fatty tissue called myelin that surrounds and protects nerve cells. When myelin is damaged, the neurons behave like electrical wires that are shorting out because they have no insulation. Myelin is the material damaged in MS.
When that happens, they can no longer send signals from the brain to the muscles. The result is blurred vision, poor coordination, slurred speech, numbness, and in the most acute cases, blindness and paralysis.
Their targets were two chemical molecules of a type called chemokines. Their normal function is to signal T-cells (T-lymphocyte cells) in the blood to tell them to repair injuries and promote recovery from illness. When there are too many of the chemokines in the central nervous system (the brain), an overwhelming number of T-cells may appear and start destroying the myelin, interfering with nerve signaling.
After the mice began to show multiple sclerosis-like symptoms, weakness of the hind legs and partial paralysis, Lane and his co-workers injected them with antibodies that may combat the action of the chemokines. They found that antibodies against one type of chemokine, called CXCL-9, did not have any effect.
But when they injected antibodies against a second chemokine, CSCL-10, they saw the loss of myelin stop and then reverse. The mice were regrowing their myelin tissue, and eventually regained the function of their hind legs. When the injections were stopped, myelin loss began again and their paralysis returned.
“We are excited by these findings,” said Lane, an assistant professor of molecular biology and biochemistry at UCI. “While this doesn’t represent a potential cure for multiple sclerosis, it does show that there are real possibilities to address the debilitating symptoms of the disease. Because of these results, we believe that there is strong evidence that the CXCL-10 molecule is the key to starting the process of demyelination.”
Lane said the results “document the feasibility of treating demyelinating diseases with antibodies, which will be our next research direction.” What is now needed, he said, is to learn more about the molecular mechanisms of myelin repair. Once we do that we may be able to develop treatment.
The research was supported by the National Institutes of Health, the National Multiple Sclerosis Society and the Reeve-Irvine Research Center at UCI. Its findings were reported in the October, 2001, issue of the Journal of Immunology.
drkoop.com
Date Published: 10/18/01
Date Reviewed: 10/18/01
