This is a first-ever finding of the link between MSP and the debilitation that patients experience in MS.
This study will be published in the June 2002 issue of Brain, published by Oxford University Press, http://brain.oupjournals.org/.
"If you could control this enzyme, you could possibly decrease the development of disease," said Isobel Scarisbrick, Ph.D., Mayo Clinic neuroscientist and lead author of this study. "Excess MSP, as is present in inflammatory central nervous system lesions such as those in MS, may promote demyelination."
Dr. Scarisbrick and colleagues discovered MSP in 1997 while she was a research fellow at Mayo Clinic in Jacksonville, Fla. They cloned MSP and developed probes and other tools to work with the enzyme and attempt to determine its role in demyelination.
In the researchers' investigation of mouse and human MS tissue, they discovered MSP's dramatic increase in inflammatory cells in actively demyelinating human MS lesions. MSP is a multifunctional enzyme, facilitating entry of inflammatory cells into the brain and also contributing to tissue destruction when overexpressed. It also may harm processes of the oligodendroglia, cells found in the central nervous system that form the myelin sheath protecting the axon, a component of nerve cells. When functioning normally, however, MSP contributes to proper oligodendroglia function.
In the MS field, researchers have made many strides in learning about the
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Contact: Lisa Copeland
newsbureau@mayo.edu
507-284-5005
Mayo Clinic
24-May-2002