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New therapy substitutes missing protein in those with muscular dystrophy
Date:5/26/2009

ng treatment to every muscle cell via gene therapy or stem cells is difficult because muscle tissue makes up such a large portion of the human body. Furthermore, the immune system may reject the cell or gene treatment because patients would treat the newly introduced cells or genes as a foreign substance.

Ervasti's method may conquer both of those problems. Upon injection, the TAT-utrophin combination spreads around the entire body efficiently and is able to penetrate the muscle cell wall to substitute for missing dystrophin. Because every cell in the body makes utrophin naturally, TAT-utrophin circumvents immunity issues associated with other therapeutic approaches.

"Our protein replacement approach most directly and simply addresses the cause of Duchenne muscular dystrophy," Ervasti said.

This new method is not a cure for muscular dystrophy. Rather, it would be a therapy most likely administered on a regular basis. If the treatment works in larger animal models and humans, it's most likely researchers would develop a drug for patients. Ervasti is hopeful the therapy can move into human clinical trials within 3 years.


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Contact: Nick Hanson
hans2853@umn.edu
612-624-2449
University of Minnesota
Source:Eurekalert

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