Multiple sclerosis (MS) is characterized by damage to our nerve fibers' “myelin sheaths,” the thick layers of specialized insulating cells that normally wrap around them.
Myelin damage causes nerve signals to be slowed, shorted, or blocked, resulting in the well-known difficulties MS sufferers have in controling the muscles to which those nerves lead.
Under normal circumstances, the myelin sheath can regenerate after damage. However, factors made by the nerve and surrounding cells regulate this regenerative capacity. Our understanding of what these factors are and how they control regeneration and remyelination is still limited.
Now, in today's issue of Neuron, a Rockefeller University research team led by Sidney Strickland reports the identification of the blood clotting factor fibrin as a critical protein in the regulation of regeneration of the myelin sheath following injury.
The body usually makes fibrin to allow the blood to clot over a wound. However, researchers have previously also observed that it accumulates in damaged nerves immediately following the injury. Such fibrin deposition is subsequently cleared, and this clearance seems to correlate with the timing of nerve regrowth and repair. Increased deposition has also been reported at the site of nerve lesions in MS patients.
Strickland and colleagues studied nerve regeneration in mice lacking fibrin. Strikingly, the mice lacking fibrin regenerated crushed nerves significantly faster than mice with fibrin.
After further investigation, the researchers discovered that this is possible because fibrin normally plays a role in keeping sheath cells in an immature state in which they are not capable of regenerating the intact myelin sheath. In the absence of fibrin, sheath cells are able to mature more quickly and can more efficiently remyelinate damaged nerves.
These results point the way toward a potentially new treatment for nerve injuries and suggest that preventing fibrin deposition may be a means to enhance the nervous system's natural regenerative capacities.
[Contact: Sidney Strickland ]