The mystery of why multiple sclerosis (MS) tends to go into remission while women are pregnant may be the secret to overcoming the devastating neurodegenerative disease, according to University of Calgary researchers who have shown that a pregnancy-related hormone is responsible for rebuilding the protective coating around nerve cells.
In a paper to be published in the February 21 issue of The Journal of Neuroscience, a team of researchers from the U of C's Faculty of Medicine reports that a study conducted on mice found that the hormone prolactin encourages the spontaneous production of myelin, the fatty substance that coats nerve cells and plays a critical role in transmitting messages in the central nervous system. A collaboration between the laboratories of Drs. Samuel Weiss and V. Wee Yong of the Hotchkiss Brain Institute, the study is the first to determine that prolactin, which increases in the body during pregnancy, is directly responsible for the formation of new myelin in the brains and spinal cords of pregnant mice. Further, when non-pregnant mice with MS-like lesions were injected with prolactin, their myelin was also repaired.
The research was based on evidence that MS, which is more common in women than men, goes into remission when women become pregnant. MS is a neurodegenerative disease where the body's own immune system attacks the myelin surrounding nerves, leading to progressive loss of sensation and movement. MS affects approximately 2.5 million people worldwide and Canadians have one of the highest rates of the disease in the world.
"It is thought that during pregnancy, women's immune systems no longer destroyed the myelin," said Weiss, director of the Hotchkiss Brain Institute and senior author of the study. "However, no previous study has tested whether pregnancy actually results in the production of new myelin, which may lead to improvement of symptoms." The paper's findings represent the first example of a na
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Contact: Grady Semmens
gsemmens@ucalgary.ca
403-220-7722
University of Calgary
20-Feb-2007