Miller School/The Miami Project to Cure Paralysis Researcher Co-Authors Nature Study
Kevin Park, Ph.D., assistant professor of neurological surgery at the Miller School’s Miami Project to Cure Paralysis, and colleagues published a manuscript in the prestigious journal Nature that demonstrates that the deletion of two genes, phosphatase and tensin homologue (PTEN) and suppressor of cytokine signaling 3 (SOCS3), promotes continued and significant axon regeneration following injury.
The study, conducted with colleagues at F.M. Kirby Neurobiology Center, Children’s Hospital Boston, and Harvard Medical School, and led by Zhigang He, Ph.D., B.M., associate professor of neurology at Harvard Medical School, was conducted on damaged optic nerves. The findings may ultimately provide an important avenue to researchers currently unraveling the mysteries of spinal cord injury and other neurodegenerative disorders since long-distance axonal regeneration has, until this point, proved difficult to attain.
“This is truly an exciting time in paralysis and central nervous system injury research,” said Miami Project Scientific Director W. Dalton Dietrich, Ph.D., the Kinetic Concepts Distinguished Chair in Neurological Surgery. “Each day we are answering more questions that provide us another piece of the puzzle. As our researchers continue to obtain more critical information, viable solutions and strategies for treating paralysis come into clearer view. We hope to move these promising therapies for testing to the clinic in the near future.”
Axons of the mammalian central nervous system typically do not regenerate after injury. Developing a strategy to promote regeneration and functional reconnection of injured axons has been a longstanding challenge, and central to The Miami Project to Cure Paralysis’ mission. This study demonstrated for the first time that simultaneous removal of both the PTEN and SOCS3 genes, which are highly expressed in injured neurons, allows sustained and robust long-distance axon regeneration in the optic nerve after injury. In addition, double deletion of these genes works synergistically to regulate activation and expression of several growth-related genes that improve axon regeneration.
Future work stemming from the finding will be directed at examining whether regenerated axons after PTEN/SOCS3 deletion can reform synapses and restore behavioral functions.