A Rockefeller University research team led by Sidney Strickland has reported the identification of the blood clotting factor fibrin as a critical protein in the regulation of regeneration of the myelin sheath following injury. MS is characterized by damage to 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 persons with MS have in controlling the muscles to which those nerves lead.

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 growth and repair. Increased deposition has also been reported at the site of nerve lesions in patients with MS.

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 the 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 regenerative capacities. www.acurian.com

This entry was posted on Tuesday, July 9th, 2002 at 4:22 pm and is filed under All Articles, Clinical Issues, Multiple Sclerosis News. You can follow any responses to this entry through the RSS 2.0 feed. Both comments and pings are currently closed.