The saying "Knowing is half the battle" is never more true than when discussing early treatment of Muscular dystrophy disease. Muscular dystrophy is one such disease where patients can benefit from early treatment. Now, new research is moving doctors and scientists closer to disease diagnosis in advance of patient symptoms.

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.

Mutations in the nuclear intermediate filament lamin A/C (LMNA) gene are associated with Emery-Dreifuss muscular dystrophy, but cause the disease by unknown mechanisms. Méjat et al. show that one mechanism involves the disruption of neuromuscular junctions.

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.

The overlooked and undervalued protein, sarcospan, just got its moment in the spotlight. Peter et al. now show that adding it to muscle cells might ameliorate the most severe form of muscular dystrophy.

A University of Iowa study suggests that the prolonged fatigue after mild exercise that occurs in people with many forms of muscular dystrophy is distinct from the inherent muscle weakness caused by the disease.

A set of new stem cell lines will make it possible for researchers to explore ten different genetic disorders—including muscular dystrophy, juvenile diabetes, and Parkinson's disease—in a variety of cell and tissue types as they develop in laboratory cultures.

A set of new stem cell lines will make it possible for researchers to explore ten different genetic disorders—including muscular dystrophy, juvenile diabetes, and Parkinson's disease—in a variety of cell and tissue types as they develop in laboratory cultures.

Researchers at the Joslin Diabetes Center have demonstrated for the first time that transplanted muscle stem cells can both improve muscle function in animals with a form of muscular dystrophy and replenish the stem cell population for use in the repair of future muscle injuries.

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