Fibrin Is Critical In Regeneration Of Myelin Sheath

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Fibrin Is Critical In Regeneration Of

Myelin Sheath

http://unisci.com/stories/20021/0314026.htm

 

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 strickland ]

 

14-Mar-2002