According to a new study, fibrin, a protein that helps form blood clots, may also be involved in regulating the repair of nerve damage. The discovery could lead to new strategies for repairing diseases of the nervous system, such as multiple sclerosis, although the research is still on the basic science level.
In multiple sclerosis, the slow destruction of myelin--the thin, protective coating that insulates nerve fibers in the brain and spine can lead to numbness, muscle weakness and stiffness, impaired vision and coordination problems. In nerves outside the brain or spinal cord, loss of myelin can also occur after an injury.
AdvertisementPrevious research has shown that fibrin gathers in the lesions of people with multiple sclerosis, but the protein's role in nerve repair has not been studied widely. Now Dr. Sidney Strickland and colleagues at Rockefeller University in New York report that fibrin seems to play a critical role in repairing damaged myelin. The researchers made the discovery by studying mice that lacked the protein. After an injury to the sciatic nerve (located in the leg), myelin regenerated much more rapidly in fibrin-free mice than in normal mice.
Strickland's team describes fibrin's role in the repair process--at least outside the brain and spinal cord. After a nerve injury, it seems that a protein called fibrinogen can leak from the blood into the damaged nerve. Once in the nerve, fibrinogen is converted into fibrin. While this is going on, myelin-repairing cells called Schwann cells begin proliferating. But the presence of fibrin keeps Schwann cells from beginning their repair job.
As fibrin is gradually dissolved, however, Schwann cells are able to begin repairing the damaged myelin and regenerating the myelin sheath as the nerve grows. Schwann cells help repair nerves outside of the brain and spinal cord, while a second type of cell has at least "limited capacity" to repair myelin in the brain.
According to him, fibrin has two effects on the repair process. As it does in other types of injury, the protein helps stop bleeding, he said. But fibrin also helps choreograph the repair process, he explained.
The presence of fibrin tells neurons and supporting cells that there has been an injury. But the repair process does not start until the injury is resolved and fibrin stops leaking in from the blood. Strickland pointed out that just as it would not make sense to refinish a damaged floor without first repairing the leaky roof, it would not make sense to begin repairing myelin until the injury was under control.
It may be possible to improve the regeneration of myelin by targeting fibrin in people with multiple sclerosis, Strickland said. He cautioned, however, that there is not yet an effective way to target fibrin that leaks into a nervous system injury without targeting fibrin throughout the body. Since fibrin is essential for blood clotting, blocking the protein throughout the body would not be a workable treatment.
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