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Friday October 19 2001Protein Gives Clue to MS, Other DiseasesBy Merritt McKinney NEW YORK (Reuters Health) - Molecules involved in inflammation have been thought to worsen multiple sclerosis (MS) and other neurological illnesses, but North Carolina researchers report that an inflammatory protein seems to play a major role in the repair of the central nervous system. If scientists can harness the repair skills of the molecule, known as tumor necrosis factor-alpha (TNF-a), they may be able to develop new treatments for MS and other diseases that damage the central nervous system, according to the report in the advance online edition of the journal Nature Neuroscience. In an interview with Reuters Health, however, one of the study's authors cautioned that any such treatments are a long way from practical use. Multiple sclerosis and many other types of neurological disease slowly destroy myelin--the thin, protective coating that insulates nerve fibers in the brain and spine. The destruction of myelin can lead to numbness, muscle weakness and stiffness, impaired vision and coordination problems. In a set of experiments in mice, researchers at the University of North Carolina at Chapel Hill studied the effects of TNF-a on the body's ability to repair myelin once it is damaged. The researchers gave cuprizone, a toxin that strips away myelin, to a group of mice that lacked the gene for TNF-a and a group of normal mice. After scientists stopped giving mice the toxin, the repair of myelin, a process called remyelination, occurred fairly rapidly in normal mice. In the mice that lacked TNF-a, however, remyelination was slower and much less complete. This is not the first time that an inflammatory molecule has been linked to myelin repair, according to Jenny P.-Y. Ting, one of the study's authors. She told Reuters Health that one of her collaborators previously made a similar discovery about interleukin-1 (IL-1), another molecule involved in inflammation. The earlier research demonstrated that a lack of interleukin-1 impairs the repair of myelin in mice, Ting explained. ``Both IL-1 and TNF-a are hallmarks of inflammation,'' Ting said. The accepted thinking, according to the North Carolina researcher, is that these two inflammatory molecules should be blocked to produce beneficial effects. The present study demonstrates, however, that ``TNF-a actually has a healing function,'' Ting said. It triggers the regeneration of cells in the brain that are needed for brain repair, she explained. ``Although unexpected, this certainly is not entirely without precedence,'' Ting said. She noted that in the immune system, molecules in the TNF family are also important for the formation of lymph organs. The research demonstrates ``that proper amounts of inflammatory molecules produced at the right time may be there for a good reason,'' Ting said. ``If we can figure out a way to harness this specific pathway, it may be possible to enhance the repair process,'' Ting said. But she added that the research is still in the early stages. ``We are far from novel therapeutics to actually help patients,'' she said. SOURCE: Nature Neuroscience advance online 2001;10.1038. Back to Top |
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