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Cell-surface sugar defects may trigger nerve damage in multiple sclerosis patients
Date:9/20/2007

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In previous studies, Demetriou found that the dietary supplement N-acetylglucosamine (GlcNAc), which is similar but more effective than the widely available glucosamine, corrected defects in protein glycosylation in cells and inhibited inflammatory demyelination in mice. The new study opens the possibility that metabolic therapy with GlcNAc may also prevent neurodegeneration. Studies in humans are required to assess the potential of this therapy in MS.


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Contact: Tom Vasich
tmvasich@uci.edu
949-824-6455
University of California - Irvine
Source:Eurekalert

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