Researchers Offer Hope to Victims of Brain Injuries and Spine Injuries
According to U.S. News and World Report, a new study may lead to new treatments for people with brain injuries and spinal cord injuries. Researchers found that they can enable the regeneration of injured nerve fibers in mice by deleting a single gene.
The researchers at the Children’s Hospital in Boston deleted the SOCS3 gene in the retinal ganglion cells in the optic nerve of mice. The SOCS3 gene is an inhibitor of the growth pathway known as mTOR. The removal of the SOCS3 gene resulted in vigorous growth of injured nerve fibers (axons). After one week, the mTOR growth pathway was reactivated. When the scientists used ciliary neurotrophic growth factor (CNTF) on the eyes of the mice, axon growth increased even more.
“CNTF and other cytokines [cellular signaling molecules] have been tested for promoting axon regeneration previously, but with no success,” said lead author Zhigang He of the F.M. Kirby Neurobiology Center at Children’s hospital Boston. “Now we know that this is due to the tight negative control of SOCS3. Inhibiting SOCS3, using small molecule compounds or RNA interference, might allow these cytokine growth factors to be functional.”
The study appears in the December 10 issue of the medical journal Neuron. It was conducted by scientists from the F.M. Kirby Neurobiology Center, the Department of Neurology at Harvard Medical School, and the Institute of Neuroscience at Carleton University in Ottawa. The abstract of the study follows:
Axon regeneration failure accounts for permanent functional deficits following CNS injury in adult mammals. However, the underlying mechanisms remain elusive. In analyzing axon regeneration in different mutant mouse lines, we discovered that deletion of suppressor of cytokine signaling 3 (SOCS3) in adult retinal ganglion cells (RGCs) promotes robust regeneration of injured optic nerve axons. This regeneration-promoting effect is efficiently blocked in SOCS3-gp130 double-knockout mice, suggesting that SOCS3 deletion promotes axon regeneration via a gp130-dependent pathway. Consistently, a transient upregulation of ciliary neurotrophic factor (CNTF) was observed within the retina following optic nerve injury. Intravitreal application of CNTF further enhances axon regeneration from SOCS3-deleted RGCs. Together, our results suggest that compromised responsiveness to injury-induced growth factors in mature neurons contributes significantly to regeneration failure. Thus, developing strategies to modulate negative signaling regulators may be an efficient strategy of promoting axon regeneration after CNS injury.
Studies on axon regeneration constitute one of the most exciting fields of scientific research. These studies give hope to the millions of people who suffer from traumatic brain injuries and spinal cord injuries. In the future, doctors may be able to repair spinal cord injuries through axon regeneration and allow new beginnings for millions of patients.
Spinal cord injuries and brain injuries are common in auto accidents as well as workplace accidents and sports accidents. If you or a family member have suffered a spinal cord injury, contact an experienced Georgia spinal cord injury attorney. You may be entitled to recovery if someone else is legally liable for the injury. Call MLN Law at 404-531-9700 to schedule a free consultation and learn more about your legal rights.