Muscular Dystrophy News -- ScienceDaily

Muscular Dystrophy News -- ScienceDaily
  • Helper molecule reverses degeneration of muscle in mouse model of tissue aging, wasting
    Maintaining proper levels of an essential helper molecule is crucial for optimal muscle function. Some athletes are already taking supplements to increase synthesis of this compound, called NAD, with the hopes of reversing the natural decay associated with aging of the mitochondria, the cell's powerhouses. However, this is the first study to directly investigate the consequences of NAD deficiency on muscle function.
  • Gene therapy developed for muscle wasting
    A discovery could save millions of people suffering from muscle wasting disease.
  • Gene controls regeneration of injured muscle by adult stem cells
    A key gene enables the repair of injured muscle throughout life, according to a study in mice. The study results further suggest that this "overlooked" gene may play an important role in sarcopenia, the loss of muscle tissues with age.
  • Protein found to bolster growth of damaged muscle tissue
    Biologists have found that a protein that plays a key role in the lives of stem cells can bolster the growth of damaged muscle tissue, a step that could contribute to treatments for muscle degeneration caused by old age or muscular dystrophy.
  • New method to grow and transplant muscle stem cells holds promise for treatment of muscular dystrophy
    Satellite cells are stem cells found in skeletal muscles. While transplantation of such muscle stem cells can be a potent therapy for degenerative muscle diseases such as Duchenne muscular dystrophy, these cells tend to lose their transplantation efficiency when cultured in vitro. Researchers treated these stem cells with leukemia inhibitory factor, which effectively maintained the undifferentiated state of the satellite cells and enhanced their transplantation efficiency.
  • Cause of heart arrhythmia in adult muscular dystrophy clarified
    The cause of heart arrhythmia in myotonic dystrophy was RNA abnormalities in the sodium channel in the heart, clarifying the symptom's mechanism, an international joint research group found. This finding will be helpful in prevention and early intervention of death in this disease, leading to the development of new treatment.
  • Cell insights shed light on how muscle-wasting disease takes hold
    Insights into how our cells control muscle development could aid understanding of muscular dystrophy and other inherited diseases, say scientists.
  • New insights into muscular dystrophy point to potential treatment avenues
    Certain stem cells in our bodies have the potential to turn into either fat or muscle. Experiments in mice suggest prospective drugs that manipulate these cells' fate could make it possible to relieve many of the symptoms of muscular dystrophy.
  • New muscular dystrophy drug target identified
    Muscle cells affected by muscular dystrophy contain high levels of an enzyme that impairs muscle repair, scientists have discovered. This finding provides a new target for potential drug treatments for the disease, which currently has no cure.
  • Origin of heart dysfunctions in myotonic dystrophy identified
    An international team of scientists is lifting the veil on the molecular mechanisms causing heart dysfunctions in myotonic dystrophy, a genetic disease affecting one person in 8,000.
  • Scientists reveal how osteopontin ablation ameliorates muscular dystrophy
    Removing an immunomodulatory protein called osteopontin improves the symptoms of mice with muscular dystrophy by changing the type of macrophages acting on damaged muscle tissue, according to a new paper. The study adds support to the idea that osteopontin inhibitors could be used to treat patients with Duchenne muscular dystrophy.
  • Face- and eye-muscle research sheds new light on Duchenne muscular dystrophy
    Researchers have investigated the biochemical and physiological characteristics of orbicularis oculi, a group of facial muscles that control the eyelids and are selectively spared or involved in different neuromuscular disorders. What they found also helps to explain why another set of muscles -- the extraocular muscles that control the movement of the eye -- are not affected by Duchenne muscular dystrophy, congenital muscular dystrophy, and aging.
  • Decoding sugar molecules offers new key for combating muscular dystrophy
    Scientists have succeeded in decoding a sugar molecule and clarifying a mechanism linked to muscular dystrophy. Their discovery has potential implications for muscular dystrophy treatment.
  • New therapeutic target for spinal muscular atrophy
    Neuroscientists have discovered a specific enzyme that plays a critical role in spinal muscular atrophy, and that suppressing this enzyme's activity, could markedly reduce the disease's severity and improve patients' lifestyles.
  • Teaching stem cells to build muscle
    Researchers have identified pecific ways in which fetal muscle stem cells remodel their environment to support their enhanced capacity for regeneration, which could lead to targets for therapies to improve adult stem cells' ability to replace injured or degenerated muscle.