High Protease Levels Contribute to MS Damage

This degradative enzyme may play an important role in the demylination process of multiple sclerosis, and drugs designed to inhibit it could potentially block the process of tissue damage. This study appears in the June 2002 issue of Brain.

MSP was discovered in 1997, and probes and other tools to work with the enzyme were developed to attempt to determine its role in demyelination.

In the current investigation two animal models that closely resemble human multiple sclerosis were studied in addition to lesions from multiple sclerosis victims. Results showed that high levels of MSP were present within infiltrating mononuclear cells, including macrophages and T cells, which characteristically fill sites of demyelination, both in human multiple sclerosis lesions and in the animal models of the disease.

"If you could control this enzyme, you could possibly decrease the development of disease,” said Dr. Isobel Scarisbrick of the Mayo Clinic (Rochester, MN, USA), and lead author of the study. "Excess MSP, as is present in inflammatory central nervous system lesions such as those in MS, may promote demyelination.” In addition, high levels of MSP may harm processes of the oligodendroglia, cells found in the central nervous system that form the myelin sheath. At normal levels, however, MSP contributes to proper oligodendroglia function.

"We are not reporting this as a cure, but it represents something that could be targeted for therapy,” says Dr. Scarisbrick. "We have a lot more work to do.”



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