"The most tragic case of this is spinal cord injury, which the medical community has never been able to effectively treat, other than to stabilize the patient. This problem has classically been considered one mainly of environment, as the central nervous system normally contains molecules that are deleterious to axonal regeneration, and even more such molecules are produced after injury. A "glial scar" forms after the spinal cord is injured wherein activated microglia induce the manufacture of chondroitin sulfate proteoglycans, which strongly deter axonal growth/regeneration. Recent studies suggest, however, that intrinsic factors in adult neurons limit the growth potential of mature axons after injury compared to the axons of developing neurons. Various strategies have been proposed to augment the capacity of injured axons to regenerate, such as treating the neurons with cocktails of growth factors and/or enzymatically digesting components of the glia scar, but such approaches have thus far not lived up to the hope that they would enable human patients to regenerate injured nerves in the central nervous system."


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"Suppressing the enzyme fidgetin promotes the re-growth of experimentally injured nerve cells and their connections, according to research with laboratory rats that will be presented Tuesday, Dec. 17, at the American Society for Cell Biology (ASCB) annual meeting in New Orleans."