New research into the activity of Schwann cells suggests that it may be possible to induce a faster transformation into “repair” mode, thereby promoting axon regrowth after physical injury and repair of nerve damage from diabetes. The study, conducted by researchers from the University of Wisconsin-Madison, focused on the mechanism by which Schwann cells, which surround axons in the peripheral nervous system, become activated and transformed following nerve injury. In this “repair” state, Schwann cells perform a variety of functions that are necessary for axon regrowth to occur. These include dissolving myelin which impedes regeneration, attracting blood cells for regrowth, mapping out the regrowth pathway, and finally, regenerating the myelin sheath on the restored axon. The findings were published August 30 in The Journal of Neuroscience.
In investigating the mechanism by which this transformation occurs, the UW-Madison team focused on the cell genes, identifying a system called PRC2 that functions as a silencer to turn off the repair function of the cell. Senior author John Svaren, PhD, professor of comparative biosciences at the UW-Madison School of Veterinary Medicine states that the team has identified an enzyme that overrides this “switch”, enabling the repair function to commence. Svaren commented “We have thought of the Schwann cell as a static entity that was just there to make myelin, but they have this latent program, where they become the first responders and initiate many actions that are required for the axon to regenerate.” Read a news story about the study findings here. The journal abstract may be read here.