June 28, 2010

Myelin repairing itself - wahoo!

Protein Helps Mitigate the Effects of Multiple Sclerosis

As well as the marks of other conditions

June 8th, 2010, 12:42 GMT
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Image showing demyelinization damage on a nerve cell
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A group of American investigators from the Washington University School of Medicine (WUSM) has recently developed a new approach to mitigating the devastating effects diseases like multiple sclerosis leave behind in the brain of patients. The science team says that a protein involved in building the cortex of children and infants could have its action hijacked, and then used to restore the mature brain to its former potential. The finding could have significant implications for a large number of people suffering from MS and other neurodegenerative conditions, the experts say.

The disease appears when myelin, the protective layer that ensures the insulation of nerve cells, is disrupted. This causes the electrical signals traveling between neurons to lose their intensity, and become scrambled. “In MS patients, myelin repair occurs inconsistently for reasons that aren't clear. Understanding the nature of that problem is a priority because when myelin isn't repaired, the chances that an MS flare-up will inflict lasting harm seem to increase,” explains WUSM associate professor of medicine and of neurobiology Robyn Klein, MD, PhD. The scientist is also the senior author of the new investigation, which is detailed in the latest online issue of the esteemed journal Proceedings of the National Academy of Sciences (PNAS).

The WUSM team conducted its recent study on a batch of unsuspecting lab mice, which were genetically modified to act as a model for multiple sclerosis. It was discovered that a protein known as CXCR is directly responsible for fixing the myelin sheet covering the neurons. The finding was made possible by the fact that the group did not use a standard MS model for the research. In past works, the actions the brain took in repairing itself were obscured by the response of the immune system. The problem was circumvented through the use of the drug cuprizone, which promotes the death of myelin-forming cells in the mouse brain.

The results were “a surprise, because the main thing CXCR4 has been known for is its role in forming the brain, not healing the brain. But we did know that injury increases the number of brain cells that make CXCR4, so it wasn't an unreasonable place to look,” Klein explains. “We do not yet know if this myelin repair pathway is somehow damaged or impaired in MS patients. But I like the idea of turning on something that the brain already knows how to make by itself, allowing it to heal itself with its own molecules,” the expert adds. The WUSM team is now about to begin a new set of investigations, in which they will look at this protein, its actions, and its potential for a new drug in deeper detail.

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