Researchers have cleared a safety hurdle in efforts to develop a gene therapy for a form of muscular dystrophy that disables patients by gradually weakening muscles near the hips and shoulders.

Muscular dystrophy, which affects approximately 250,000 people in the United States, occurs when damaged muscle tissue is replaced with fibrous, bony or fatty tissue and loses function. While scientists have identified one protein, dystrophin, as an important piece to curing the disease, another part of the mystery has eluded scientists for the past 14 years.

Current research suggests laminin, a protein that helps cells stick together, may lead to enhanced muscle repair in muscular dystrophy. The related report by Rooney et al, "Laminin-111 restores regenerative capacity in a mouse model for alpha 7 integrin congenital myopathy," appears in the January 2009 issue of The American Journal of Pathology.

By injecting purified stem cells isolated from adult skeletal muscle, researchers have shown they can restore healthy muscle and improve muscle function in mice with a form of muscular dystrophy.

New study in the FASEB Journal identifies c-FLIP and calpain-3 proteins as drug targets in limb-girdle muscular dystrophy and other conditions

New research from the University of Virginia Health System shows that, in cases of Type 1 myotonic muscular dystrophy (DM1), a well known heart protein does several surprising things. DM1 is the most common form of muscular dystrophy in adults and affects approximately 40,000 adults and children in the U.S.

The production of utrophin slows in fetal muscles soon after birth, after which dystrophin takes over as the primary muscle-associated protein. How this normal utrophin silencing occurs has been a mystery, until now.