Duchenne muscular dystrophy (DMD) is a progressive muscle disorder that causes the loss of both muscle function and independence. DMD is perhaps the most prevalent of the muscular dystrophies and is the most common lethal genetic disorder diagnosed during childhood today. Each year, approximately 20,000 children worldwide are born with DMD (one of every 3,500 male children).
Scientists in the United States say an experimental drug may be able to compensate for the genetic error responsible for some cases of Duchenne Muscular Dystrophy (DMD) and cystic fibrosis.
Scientists at Dana-Farber Cancer Institute have shown in a laboratory study that revving up a crucial set of muscle genes counteracts the damage caused by a form of muscular dystrophy.
In the April 1st issue of Genes & Development, Dr. Bruce Spiegelman (Dana Farber Cancer Institute) and colleagues identify a key genetic component of and possible therapeutic target for Duchenne muscular dystrophy.
Some of the world's leading doctors and scientists will join together in a multi-million pound international network aimed at improving treatment and finding cures for thousands of patients with debilitating neuromuscular diseases.
Italian scientists, by using new stem cell therapy on dogs with muscular dystrophy, have improved the dogs condition to such an extent that the dogs were able to walk and even jump again.
A powerful new method of testing embryos for inherited diseases, has been developed by fertility specialists in Britain.
New approaches to genetic disease, based on cells' own ability to correct themselves, will be outlined today at the annual conference of the European Society of Human Genetics in Amsterdam, The Netherlands.
The clinical trial for Duchenne muscular dystrophy (DMD) tests the safety and effectiveness of a therapy that was developed over two decades by scientists at the University of North Carolina Chapel Hill's School of Medicine and the University of Pittsburgh.
In experiments with transgenic mice, University of Pennsylvania School of Medicine researchers discovered the remaining steps in the complicated process of how the largest class of jumping genes replicates and inserts themselves within the human genome.
In a surprising discovery with implications for treating muscular dystrophy, researchers at the University of Utah School of Medicine and other institutions have identified a major source of origin for two groups of adult cells that regulate muscle repair.
Researchers at the University of Minnesota Medical School have discovered the gene responsible for a type of ataxia, an incurable degenerative brain disease affecting movement and coordination.
New research shows that a wasting condition responsible for nearly a third of all cancer deaths involves the loss of an essential muscle protein that is also lost in people with muscular dystrophy.
Cardiac disease, particularly dilated cardiomyopathy and heart failure, is the major cause of mortality in patients with muscular dystrophy and is present in most boys with Duchenne muscular dystrophy and approximately 70 percent of those with Becker muscular dystrophy. These are the two common forms of muscular dystrophy caused by defects in a gene called dystrophin.
Adult stem cells taken from bone marrow are the "shooting stars" of their field. Many research scientists have been speculating that the cells might be able to pass through the blood into diseased organs and replace defective tissue. Such cells are seen as the potential key to the treatment of certain muscle diseases.
A common chemical used in the manufacturing and pharmaceutical industries can repair damage to cardiac muscle cell membranes and prevent heart failure in mice with the genetic mutation that causes Duchenne muscular dystrophy, according to scientists at the University of Michigan Medical School.
Skeletal muscles naturally repair themselves very efficiently after injury. But when they don’t, otherwise successful recovery following damage from overuse during exercise, surgery or trauma can be stymied. Furthermore, as we age, muscle repair slows noticeably, and in Duchenne Muscular Dystrophy and other degenerative muscle diseases, normal repair functions can’t cope with disease progression.
A new study from Karolinska Institutet in Stockholm shows that hundreds of genes in the thigh muscle are activated in regular cycle training. The study also reveals that great differences in training response may be due to the ability in some people to activate their genes much more forcefully. The study is published May 2 in FASEB Journal.
Corticosteroids can be beneficial in the treatment of Duchenne muscular dystrophy and can be offered as a treatment option, according to the American Academy of Neurology and the Child Neurology Society in a new practice guideline published in the January 11 issue of Neurology, the scientific journal of the American Academy of Neurology.
Researchers at the University of Pennsylvania School of Medicine report a novel strategy for stimulating the production of utrophin – an important muscle protein in young mice – for muscular dystrophy therapy.
MDA-supported researchers at the University of Washington-Seattle have delivered the gene for the dystrophin protein to all voluntary muscles with a single intravenous injection in mice with Duchenne muscular dystrophy (DMD).