Journal
NEUROLOGICAL RESEARCH
Volume 30, Issue 10, Pages 1047-1052Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1179/174313208X362523
Keywords
Axon regeneration inhibitor; brachial plexus; ganglioside; nerve regeneration; sialidase
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Funding
- National Institutes of Health [R37NS037096, R21NS046669]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R21NS046669, R37NS037096] Funding Source: NIH RePORTER
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Objective: To increase awareness of the advancements in nerve regeneration. Methods: Review of the literature regarding inhibitors of nerve outgrowth and presentation of potential agents that reverse the inhibition, thereby promoting nerve regeneration. Results: The injured adult central nervous system (CNS) inhibits axon outgrowth, thereby limiting recovery from traumatic injury. Axon regeneration inhibitors (ARIs) that contribute to inhibition of recovery include myelin-associated glycoprotein, Nogo, oligodendrocyte-myelin glycoprotein and chondroitin sulfate proteoglycans. The ARIs bind to specific receptors on the axon growth cone to halt outgrowth; consequently, reversing or blocking the actions of ARIs may promote recovery after CNS injury. Sialidase, an enzyme that cleaves one class of axonal receptors for myelin-associated glycoprotein, enhances spinal axon outgrowth into implanted peripheral nerve grafts in a rat model of brachial plexus avulsion, a traumatic injury in which nerve roots are torn from the spinal cord. Conclusion: Repair using peripheral nerve grafts is a promising restorative surgical treatment in humans, although functional improvement remains limited. Molecular therapies targeting ARIs may aid functional recovery after brachial plexus avulsion or other nervous system injuries and diseases. [Neurol Res 2008; 30: 1047-1052]
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