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Multiple sclerosis in humans has not responded well to drugs that block tumor necrosis factor-alpha (TNF-alpha), despite evidence that TNF-alpha contributes to the damage in animal models of the disease. A paper in the November issue of Nature Neuroscience now reports that TNF-alpha has two opposite effects in mice, first accelerating damage to axons and later accelerating its repair. This finding may explain the discrepancies between laboratory and clinical studies, and thus aid the development of more effective treatments for the disease.
In multiple sclerosis, the patient's immune system destroys oligodendrocytes, the insulating cells that surround axons, thus reducing the neurons' ability to communicate with each other. Oligodendrocytes can grow back, however, and increasing their rate of repair is a promising treatment approach. In the new paper, Jenny Ting and colleagues at the University of North Carolina show that mice lacking the gene for TNF-alpha or one of its receptors show less initial damage in response to a drug that kills oligodendrocytes, as expected from previous work. Surprisingly, though, the mutant mice were much slower to repair the damage, apparently because proliferation of this cell type requires TNF-alpha signals. This suggests that the effectiveness of therapies involving the TNF-alpha pathway may vary based on the timing of drug treatment. Author contact: Dr. Jenny P.-Y. Ting
UNC Lineberger Comprehensive Cancer Center
Chapel Hill, USA
Tel: +1 919 966 6538
E-mail panyun@med.unc.edu (C) Nature Neuroscience press release.
Message posted by: Trevor M. D'Souza
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