Researchers at the National Institute of Neurological Disorders and Stroke have found that boosting the transport of mitochondria along neuronal axons actually increases the likelihood of mouse nerve cells to repair themselves when faced with injury. The complete study was published in The Journal of Cell Biology and suggests a potential new strategy in order to stimulate the regrowth of human neurons that have been damaged either by disease or injury.

Neurons require a large amount of energy in order to extend their axons lengthy distances inside of the body. This energy (adenosine triphosphate) is offered by the mitochondria, which is like the internal power plant of each cell. As mitochondria develop, they are transported up and down axons in order to generate ATP when it is needed. Mitochondria in adults are not as mobile as they mature due to a protein known as syntaphilin that holds mitochondria in their current place. Zu-Hang Sheng and his colleagues at the National Institute of Neurological Disorders and Stroke questioned whether this decrease in mitochondrial movement may be able to explain why so many adults have neurons that are not able to regrow after they have been injured.

Sheng and his research fellow Bing Zhou, who was the first author of the study, found that when the axons are severed on a mature mouse, neighboring mitochondria are damaged and are then unable to provide enough ATP to support nerve regeneration. When researchers genetically removed syntaphilin from nerve cells, mitochondria transport increased. Damaged mitochondria were replaced with healthy counterparts that were more than capable of producing ATP. Syntaphilin-deficient mature neurons were again able to regrow upon injury, as they were when they were young. Removing syntaphilin from adult mice caused sciatic nerves to regenerate after injury.

Sheng says their in vivo and in vitro studies suggest that activating an intrinsic growth program requires the coordinated modulation of mitochondrial transport and recovery of energy deficits. These approaches, when combined, may actually lead to a therapeutic strategy that will allow regeneration in the central and peripheral nervous systems after injury or disease.