Sugar Molecule May Play Key Role in Muscular Dystrophy Treatment

Sugar Molecule May Play Key Role in Muscular Dystrophy Treatment

Researchers at Japan’s Kobe University Graduate School of Medicine have successfully decoded a sugar molecule, providing an important step toward understanding a mechanism linked to muscular dystrophy (MD). The study, “Identification of a Post-translational Modification with Ribitol-Phosphate and Its Defect in Muscular Dystrophy,” was published in the journal Cell Reports.

The study was led by Prof. Tatsushi Toda, Ph.D., Division of Neurology and Molecular Brain Science at the Kobe University Graduate School of Medicine. Toda’s research is focused on the identification and functional analysis of genes associated with diseases such as muscular dystrophies and Parkinson’s, and the understanding of the molecular pathogenesis of these diseases, with the goal to develop diagnostics and novel therapies.

Toda and his team created a sugar molecule in cell culture, a method of growing cells outside a living organism. Using mass spectrometry analysis, an experimental technique that sorts ions based on their mass-to-charge ratio, the researchers calculated the mass of each component in the sugar molecule and discovered an interesting sugar unit called “ribitol 5-phosphate,” which was not thought to be part of the composition of mammalian sugar structures. Previously, scientists thought it lived in bacteria and some plants.

With additional analysis the researchers discovered this sugar molecule was implicated in the cause of conditions attributable to muscular dystrophy.

“Sugar molecules play a key role in many biological processes, but their composition is difficult to determine and research on them is still limited,” Toda said in a news release. “The decoding of this sugar molecule has implications for the field of life sciences, as well as being a step further in the treatment of muscular dystrophy.”

Toda suggests this sugar unit in an abnormal state could potentially play a role in cancer metastasis and viral infection, in addition to muscular dystrophy.

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