Roundworms are hardly visible and hardly resemble people, but they are responsible for some of the leading research on Duchenne Muscular Dystrophy (DMD).
Illinois State University Assistant professor of molecular neuroethology Andres Vidal-Gadea is leading the way in DMD research along with his graduate, undergraduate and high school students assisting him.
DMD is the most well-known type of muscular dystrophy, which is a disease involving the gradual loss of strength and mobility.
In a previous interview with the Vidette, Vidal-Gadea explained some of his findings with the worms that were published in the Proceedings of the National Academy of Science journal.
Roundworms can be used to study muscular dystrophy and test therapies for preventing it. Since roundworms share two-thirds of the same genes as humans and grow muscle in the same way, Vidal-Gadea and his team can observe how the muscle forms under different types of exercise.
Their study found that while changes in intensity in exercise affected the growth rate of muscles, muscular dystrophy still progressed at the same rate.
“Our results suggest that one must look beyond simply measuring muscle growth in order to evaluate the potential success of therapeutic approaches,” Vidal-Gadea said.
Vidal-Gadea and his team found that strengthening the muscle of worms with DMD actually caused the worms to die faster.
“It’s like trading the engine in your old, beater car for a suped-up engine,” Vidal-Gadea said on exercise in muscular dystrophy patients. “The problem is what’s broken in muscular dystrophy is not that, it’s the chassis. It’s the part that transmits that force to the outside.”
Strengthening of muscles is the current area of study in human cases of muscular dystrophy. Research by Vidal-Gadea and his team shows that if strengthening worms causes them to die faster, the treatment isn’t likely to work for humans, but something on a molecular level may.
When using therapies that have exercise as a treatment for DMD, patients end up trading their health at the opportunity of getting better. Patients risk the remaining mobility they have to try new treatments.
The research done by Vidal-Gadea and his team does more than disprove current forms of DMD treatment, it also suggests areas of further study for the disease.
DMD is caused by the muscles in a person being unable to regulate calcium. Fully functioning human muscle will release calcium as muscles contract. However, in DMD patients the calcium will not leave the muscle after contracting. Over time, the calcium will build and the muscle cells will be in danger.
These findings contradict previous research that would only measure muscle growth in DMD patients and shifts the study of DMD towards a whole new direction.