Introducing the p45 protein (green) to the p75 protein (red), could trigger nerve repair in humans, paving the way for new treatments for paralysis.
Image credit: Salk Institute for Biological Studies
The research team, including senior author Kuo-Fen Lee, a professor at Salk, recently published their findings in the journal PLOS Biology.
Many creatures, such as dogs, whales, snails and frogs, have the ability to repair nerves after injury - a process that researchers have been striving to mimic in humans.
Last year, Lee and colleagues published a study in the journal PLOS One revealing that a protein called p45 activates nerve regeneration in these animals by stopping myelin - the protective coating around nerve fibers (axons) - from halting nerve regrowth.
But they found that humans and primates do not possess the p45 protein. Instead, they have a protein called p75, which attaches itself to myelin when nerves are damaged and prevents their repair.
The team's latest study investigated this process in more detail and looked at how introducing the p45 protein could encourage nerve repair.
Nerve repair process of some animals 'could be mimicked in humans'
Lee and colleagues discovered that nerve repair is halted in humans as a result of two p75 proteins, which team up and attach to nerve repair inhibitors released from damaged myelin.
Using nuclear magnetic resonance (NMR) technology, the team was able to closely analyze the configurations of the two p75 proteins. By introducing the p45 protein - which promotes nerve regeneration - they found it could break up the pairing of the p75 proteins.
In addition, the researchers discovered that the p45 protein could bind to the exact region in the p75 protein that is responsible for their pairing. This reduced the number of p75 pairs that attach to the nerve repair inhibitors released from damaged myelin, meaning nerve fibers were able to regenerate.
Based on these findings, Lee and colleagues say that p45, or another molecule that interferes with p75, could offer a potential treatment for individuals who have severe spinal cord damage and paralysis.
"This research implies that we might be able to mimic neuronal repair processes that occur naturally in lower animals, which would be very exciting."
He notes that the p45 protein could be introduced to injured nerve cells, for example, or a small molecule could be delivered to block the link between the two p75 proteins. "Such an agent could possibly get through the blood-brain barrier and to the site of spinal cord injuries," Lee adds.
Whether introducing the p45 protein could trigger nerve regeneration in humans remains to be seen, but the team says this is something they hope to find out with further research.
Earlier this year, Medical News Today reported on a study published in the journal Brain, which revealed how a spinal shock treatment helped four paralyzed men regain voluntary movement in their legs.