Damaged Neurons Can Be Repaired Through Mobilization Of Mitochondria
The study “Facilitation of Axon Regeneration by Enhancing Mitochondrial Transport and Rescuing Energy Deficits”, which appears in The Journal of Cell Biology, suggests potential new strategies to stimulate the regrowth of human neurons damaged by injury or disease. Scientists at the National Institute of Neurological Disorders and Stroke have discovered that boosting the transport of mitochondria along neuronal axons enhances the ability of mouse nerve cells to repair themselves after 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.Dr. Sheng and his research fellow, Bing Zhou, Ph.D., the first author of the study, initially found that when mature mouse axons are severed, nearby mitochondria are damaged and become unable to provide sufficient ATP to support injured nerve regeneration. However, when the researchers genetically removed syntaphilin from the nerve cells, mitochondrial transport was enhanced, allowing the damaged mitochondria to be replaced by healthy mitochondria capable of producing ATP. Syntaphilin-deficient mature neurons regained the ability to regrow after injury, just like young neurons, and removing syntaphilin from adult mice facilitated the regeneration of their sciatic nerves 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.
