INDIANAPOLIS, Ind. (WLNS) – Damaged nerve fibers that can be caused from a spinal cord injury could lead to permanent loss of function.

A lot of research has been done to find ways to regenerate nerve fibers, called axons, after an injury, but a recent study between the National Institutes of Health and the Indiana University School of Medicine may be the first step in restoring movement on previously injured axons.

Results of a study performed in mice and published in Cell Metabolism suggest that increasing energy supply within these injured spinal cord nerves could help promote axon regrowth.

“We are the first to show that spinal cord injury results in an energy crisis that is intrinsically linked to the limited ability of damaged axons to regenerate,” said Zu-Hang Sheng, Ph.D., senior principal investigator at the NIH’s National Institute of Neurological Disorders and Stroke and a co-senior author of the study.

Like gasoline for a car, the cells of the body use a chemical compound called adenosine triphosphate, or ATP, for fuel.

The ATP is mainly made by cellular power plants called mitochondria and in spinal cord nerves, mitochondria can be found along the axons.

When axons are injured, the nearby mitochondria are often damaged as well, impairing ATP production in injured nerves.

“Nerve repair requires a significant amount of energy,” said Dr. Sheng. “Our hypothesis is that damage to mitochondria following injury severely limits the available ATP, and this energy crisis is what prevents the regrowth and repair of injured axons.”

In Adults, mitochondria are anchored in place within axons which makes it difficult to replace them.

Previous study found that lacking the protein Syntaphilin allows mitochondria to freely move throughout axons.

“We proposed that enhancing transport would help remove damaged mitochondria from injured axons and replenish undamaged ones to rescue the energy crisis” said Dr. Sheng.

The Sheng lab collaborated with Xiao-Ming Xu, M.D., Ph.D. and colleagues from the Indiana University School of Medicine, who are experts in modeling multiple types of spinal cord injury.

“Spinal cord injury is devastating, affecting patients, their families, and our society,” said Dr. Xu. “Although tremendous progress has been made in our scientific community, no effective treatments are available. There is definitely an urgent need for the development of new strategies for patients with spinal cord injury.”

Mice without Syntaphilin had much more axon regrowth in multiple models as well newly grown axons that were necessary beyond the injury site.

Researchers also saw that the regrowth aided in functional recovery such as fine motor tasks in mouse forelimbs and fingers.

Further testing found that giving the mice creatine, a compound that enhances the formation of ATP, increased axon regrowth.

“We were very encouraged by these results,” said Dr. Sheng. “The regeneration that we see in our knockout mice (one without Syntaphilin) is very significant, and these findings support our hypothesis that an energy deficiency is holding back the ability of both central and peripheral nervous systems to repair after injury.”

Dr. Sheng points out that these findings are limited by the need to genetically manipulate mice.

Mice that lack Syntaphilin show long-term effects on regeneration, while creatine alone only shows slight regrowth.

Future research is required for effective energy production treatment of traumatic brain or spinal cord injury.