A team including MDA grantee Gordon Lynch in the Department of Physiology at the University of Melbourne in Victoria, Australia, found that a biological signaling pathway may help explain why mice with Duchenne muscular dystrophy (DMD) can regenerate their muscles much better than can humans with the same disease. It seems that, in mice, the biochemical pathway under the control of the protein calcineurin may be more effective than in humans.
When the investigators blocked calcineurin signaling in DMD-affected mice with the drug cyclosporine, the mice experienced muscle degeneration much more like that seen in human patients. The cyclosporine-treated mice showed much more severe muscle loss than did DMD-affected mice not treated with it.
The investigators, who published their paper online Jan. 16 in Acta Neuropathologica, suggest that enhancing calcineurin signaling or its downstream effects could be a treatment approach in DMD.