Recently, researchers at the University of Missouri (MU) found that the disruption in communication between nerves and muscles in mice causing degeneration of motor neurons parallels the same degeneration in movement that occurs within human beings suffering from Spinal Muscular Dystrophy (SMA). Michael Garcia PhD (pictured at right), associate professor of biological sciences at MU’s college of arts and science and the Bond Life Sciences Center, explains that learning where the breakdown in communication occurs between the motor neuron and muscle is key in targeting treatments to prevent SMA.
The root cause of SMA is a protein deficiency present in all cells—including motor neurons—which causes the degeneration of skeletal muscles. Motor neurons are the facilitators of the communication with the muscle, which function by releasing a complex series of chemical signals. A disruption in that communication means motor neurons stop working and muscle activity ceases. The way in which the nerve “talks” to the muscle becomes fragmented. Muscles will not function correctly when the message sent by nerves to muscles is disrupted before it arrives at a nerve ending. As a result, muscles stop functioning and movement is impaired. Slowly the body loses its ability to walk, sit or stand. Ultimately, the ability to move at all is destroyed.
Garcia explains that this discovery could lead to the treatment of SMA as well as diseases involving motor neurons including ALS and the dysfunction of the synapses that occur in Duchenne Muscular Dystrophy. There is currently no effective treatment for SMA.
Details of the study appear in the September 2011 issue of ACTA Nueropathology.
