In a study on rodents, Gail Lewandowski and Oswald Steward achieved this breakthrough by turning back the developmental clock in a molecular pathway critical to the formation of corticospinal tract nerve connections and providing a scaffold so that neuronal axons at the injury site could grow and link up again.
Results appear in the July 23 issue of The Journal of Neuroscience.
The work expands on previous research at UCI. In 2010, Steward helped discover that axons flourish after the deletion of an enzyme called PTEN, which controls a molecular pathway regulating cell growth. PTEN activity is low during early development, allowing cell proliferation. PTEN subsequently turns on, inhibiting this pathway and precluding any ability to regenerate.
Two years later, a UCI team found that salmon fibrin injected into rats with spinal cord injury filled cavities at the injury site, giving axons a framework in which to reconnect and facilitate recovery. Fibrin is a stringy, insoluble protein produced by the blood clotting process and is used as a surgical glue.
"This is a major next step in our effort to identify treatments that restore functional losses suffered by those with spinal cord injury," said Steward, professor of anatomy & neurobiology and director of the Reeve-Irvine Research Center, of the current findings. "Paralysis and loss of function from spinal cord injury has been considered irreversible, but our discovery points the way toward a potential therapy to induce regeneration of nerve connections."Full Post!