How does the functions of the muscles effect Muscular Dystrophy?? And what could be done to increase muscle function?? MY QUESTION(S):

Muscular dystrophy is a disease that effects the amount of function of the muscles. By the muscles functioning less, and therefore weakening, a person is unable to use their muscles as often as normal. Therefore the muscle weakening of this disorder is also caused by a person lack of usage of their muscles. This significant decrease in muscle function is a result of a deletion in gene dystrophin. Normal dystrophin is responsible for playing a central role in the neuromuscular junction which controls excitation/contraction coupling. The gene responsible for causing Duchenne Muscular Dystrophy, which is found on the X chromosome (reason for it mostly effecting males, inherited from mother), includes the protein—dystrophin. Dystrophin is also required inside muscle cells for support; it is said to strengthen muscle cells by fastening elements of the internal cytoskeleton to the exterior of the muscle membrane. A person lacking this protein, their cell membrane becomes permeable, and this allows many extracellular components enter the muscle’s membrane thus, increasing the internal pressure causing the muscle cell to expand greatly and result in death. And with all this, the result is decrease muscle function which than leads to muscle degeneration. I believe that the limited muscle function associated with muscular dystrophy could also be formed from a person a having a decreased rate of cellular respiration. Cellular respiration is the process which glucose is made into ATP (catabolic-breaking down). It is logical to think that a person with muscular dystrophy would not have to ability to break down glucose in order to the regular amount of ATP. The reason for this is because ATP is used for muscle contractions. And if there is not enough ATP the muscles can not complete contraction properly (sliding filament model). Therefore, I believe that cellular respiration in the mitochondria of muscle cells, is significantly decreased in muscular dystrophy patients. Also, the limited muscle function could be associated with the signaling from the brain to the muscle. A muscular dystrophy patient could have damaged dendrites which are not picking up the signaling and sending it to the muscle, which therefore result in no muscle movement. And with that continuing for a extended amount of time you than decrease usage and therefore adds to muscle weakening. Also, limited muscle function could be from a damaged cerebellum, maybe they are missing the protein that codes of normal functioning of cerebellum. And since the cerebellum is responsible for balance, muscle movement, joints, etc it makes sense that a mutated cerebellum could be cause for the limited muscle function.

Researchers and scientists are trying many things. The have tried steroids, enzyme treatment, gene therapy and much more. One of, what I believe could be, the most successful research would be the gene therapy involving the utrophin. This gene is a relative of the dystrophin protein. The only difference is the slight, in length. Dystrophin is slightly longer. Researchers have tested this on mice. If they increase the amount of utrophin in the body, this is act a replace the deletion portion dystrophin. And since these gene are extremely similar in their function it would serve to possibly increase the lost muscle function. Another thing that I think could be done to increase muscle function is increase cellular respiration. Although many environmental factors could serve to increase respiration, many muscular dystrophy patients may not have the opportunity to do those things (limited movement). In order to increase cellular respiration and person could either eat a diet containing more sugar or receive a shot. However, that may not be good for the rest of the body. But, by increasing the amount glucose (sugar) you therefore have more glucose to break down and therefore more ATP can be produced in the mitochondria of the muscle cells. Back to Main