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New prospects for treating muscular dystrophy: Stem cells restore muscle in MD mice

This news release is also available in Italian.

A study on mice suggests that a type of stem cells found in blood vessels may someday be able to regenerate wasting muscle in muscular dystrophy (MD) patients.

The authors caution that more research must be done before researchers consider applying these findings to humans. Nonetheless, their results provide a possible new direction for efforts that have met largely with frustration thus far. The study appears in the journal Science, published by AAAS, the science society.

The research team, led by Giulio Cossu of the Stem Cell Research Institute of the Scientific Institute San Raffaele, Milan, and the University of Rome and the Institute of Cell Biology and Tissue Engineering, in Rome, has found that these stem cells can cross from the bloodstream, into muscle tissue. There, they seem to take on a new identity, helping to generate new muscle fibers in mice with MD-like symptoms.

MD is a collection of disorders caused by genetic defects that lead to increasing muscle weakness over time. These disorders currently have no cure.

"Although these results are exciting, we have not cured the mice," Cossu said. "We believe this is a significant step toward therapy, but the question that keeps me awake at night is whether this will work in larger animals."

Cossu's team conducted its experiments on mice with the same genetic defect that causes one form of MD in humans. If the same stem cells, called "mesoangioblasts," can be collected from human MD patients, and if the cells have the same versatility they do early in life, they may offer a new avenue for treating the disease.

The approach Cossu and his colleagues are envisioning would involve collecting mesoangioblasts from a patient's blood vessels, genetically "correcting" the cells in the laboratory, allowing them to multipl
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Contact: Ginger Pinholster
gpinhols@aaas.org
202-326-6421
American Association for the Advancement of Science
10-Jul-2003


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