Mobilizing mitochondria may be key to regenerating damaged neurons
News Jun 07, 2016
Researchers at the National Institute of Neurological Disorders and Stroke (NINDS) have discovered that boosting the transport of mitochondria along neuronal axons enhances the ability of mouse nerve cells to repair themselves after injury. The study which has been published in The Journal of Cell Biology, suggests potential new strategies to stimulate the regrowth of human neurons damaged by injury or disease.
Neurons need large amounts of energy to extend their axons long distances through the body. This energy—in the form of adenosine triphosphate (ATP)—is provided by mitochondria, the cell's internal power plants. During development, mitochondria are transported up and down growing axons to generate ATP wherever it is needed. In adults, however, mitochondria become less mobile as mature neurons produce a protein called syntaphilin that anchors the mitochondria in place. Zu-Hang Sheng and colleagues at the NINDS wondered whether this decrease in mitochondrial transport might explain why adult neurons are typically unable to regrow after injury.
Sheng and his research fellow Bing Zhou, 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 therefore 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.
Learn More: Sugar rush shrinks brain cell powerhouse
"Our 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. Such combined approaches may represent a valid therapeutic strategy to facilitate regeneration in the central and peripheral nervous systems after injury or disease," Sheng says.
Note: Material may have been edited for length and content. For further information, please contact the cited source.
Zhou B et al. Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits. Journal of Cell Biology, Published Online June 7 2016. doi: 10.1083/jcb.201605101
All in a Droplet: Atomic Resolution of ALS Protein ResolvedNews
Researchers have described atom-by-atom changes in a family of proteins linked to amyotrophic lateral sclerosis (ALS), a group of brain disorders known as frontotemporal dementia and degenerative diseases of muscle and bone.READ MORE
Pupil Size Couples to Cortical States to Protect Deep Sleep StabilityNews
Researchers have found that mice pupil size fluctuates during sleep. They also show that pupil size is a reliable indicator of sleep states.READ MORE
A Place to Think: Persistent neuronal activity in human prefrontal cortex links perception and actionNews
Neuroscientists have tracked the progress of a thought through the brain, showing clearly how the prefrontal cortex at the front of the brain coordinates activity to help us act in response to a perception.READ MORE