There is no known cure for<unk>  yet. Treatment is aimed at control of symptoms to maximize the quality of life which can be measured by specific questionnaires. Activity is encouraged. Inactivity (such as bed rest) or sitting down for too long can worsen the muscle disease. Physical therapy may be helpful to maintain muscle strength. Orthopedic appliances such as braces and wheelchairs may improve mobility and self-care. Immunosuppressant steroids have been known to help slow the progression of<unk> . The drug prednisone contributes to an increased production of the protein utrophin which closely resembles dystrophin, the protein that is defective in<unk> . The cardiac problems that occur with EDMD and myotonic muscular dystrophy may require a pacemaker. The investigational drug Debio-025 is a known inhibitor of the protein cyclophilin D, which regulates the swelling of mitochondria in response to cellular injury. Researchers decided to test the drug in mice engineered to carry MD after earlier laboratory tests showed deleting a gene that encodes cycolphilin D reduced swelling and reversed or prevented the disease's muscle-damaging characteristics. According to a review by Bushby, et al. if a primary protein is not functioning properly then maybe another protein could take its place by augmenting it. Upregulation of compensatory proteins has been done in models of transgenic mice.
Becker muscular dystrophy
Limb–girdle muscular dystrophy
Fukuyama congenital muscular dystrophy
Duchenne muscular dystrophy
Ullrich congenital muscular dystrophy
Jokela type spinal muscular atrophy
Myotonic dystrophy
Distal spinal muscular atrophy type 2