New Clinical Care Research in SCI: Reduction of Muscle Wasting by Motoneuron Replacement

New Clinical Care Research in SCI:
Reduction of Muscle Wasting by Motoneuron Replacement

Musle fibers with no atrophy (left). After transplantation with growth factor, muscle fibers were larger (right) than fibers that had no nerve supply and no treatment (center).

Motoneurons are cells that live in the spinal cord. The messages that these neurons receive from the brain and the limbs are relayed to muscles so that they can contract. The contractions are weaker if the muscle has wasted (atrophied), a secondary complication that often occurs following spinal cord injury (SCI). This atrophy can arise when the injury or disease damages the motoneurons and the muscles lose their connections to the nervous system. In a course of studies supported by The Alan T Brown Foundation to Cure Paralysis, Christine Thomas, Ph.D. at The Miami Project to Cure Paralysis, is conducting studies that may lead to a treatment that would replace motoneurons and therefore help reduce muscle atrophy.

The strategy proposed by Dr. Thomas is to provide an alternative source of cells to restore nerve connections to the muscles. She and her colleagues have transplanted embryonic spinal cord cells into nerves near the atrophied muscles. Many of the cells they transplanted survived and produced nerve fibers that grew back to supply the muscles. The muscles also functioned when the transplanted motoneurons were electrically stimulated. This novel strategy provides the potential to excite these muscles artificially to produce simple behaviors. It also represents and alternative avenue to alleviate muscle atrophy.

Recent results from this group are promising. They have shown that by adding different growth factors to the cells at the time of cell transplantation there was less muscle wasting. To carry out the next phase of the study, The Alan T Brown Foundation will cover the costs of specialized equipment needed to observe the junctions between the transplanted cells and the muscle. In these studies Dr. Thomas and colleagues will aim to optimize the wasting of the muscles. They will also test whether these larger muscle fibers lead to stronger contractions of the muscles.

Should these strategies prove to be effective in laboratory experiments, their application in human SCI may restore lost nerve connections to muscles.

If this can be accomplished, atrophy of these muscles may be prevented and future treatments to restore voluntary function to the muscle may be enhanced.