Regeneration Blockers May Affect Myelin Levels

Many researchers have known that a number of neuronal diseases such as multiple sclerosis may be connected to the level of myelin in the body. Myelin is an insulating substance known to protect nerve fibers. People with MS are known to experience myelin damage, although the actual causes of such a disease remain unknown.

Researchers from Institute for Bioengineering of Catalonia (IBEC) may have discovered a new group of interacting partners with myelin associated receptors that might shed some light on the imbalance of production of the said substance. The group of researchers, led by Jose Antonio del Rio along with Vanessa Gil and Franc Llorens, were looking at axons, ligands and receptors in the central nervous systems in mammals. Axons are known to have a limited capacity to regenerate following any related injury. This limitation has been attributed to myelin-associated inhibitors or MAI’s.

By trying to block this myelin inhibition, the researchers believe that neuronal regeneration may improve. The IBEC researchers may have found a possible way to do so. They discovered that blocking two of some of the protein’s shared receptors may help prevent the inhibitors from restricting axonal sprouting that limits the regeneration of the damaged fiber tracts.

Although there are other elements in the myelin inhibitory pathway that remains unclear, the discovery of the roles and functions of the inhibitory molecules may further help shed light in research into neuroregeneration. Jose Antonio says, “Potentially there could be new physiological roles for them in other processes such as development, neuronal homeostasis, plasticity and neuroregeneration. Modifications could be considered as markers for certain neuronal diseases.”

Source: IBEC – Institute for Bioengineering of Catalonia. “Beating the Regeneration Blockers: New Group of Interacting Partners for Myelin-Associated Receptors.” ScienceDaily, 12 November 2010. Web. 15 November 2010. <http://www.sciencedaily.comĀ­ /releases/2010/11/101112083919.htm>

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