Axon regeneration inhibitors.

Lynda J-S Yang, Ronald L Schnaar
Author Information
  1. Lynda J-S Yang: Department of Neurosurgery, University of Michigan Health System, Ann Arbor, MI 48109-5338, USA. ljsyang@med.umich.edu

Abstract

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.

Grants

  1. R01 NS037096/NINDS NIH HHS
  2. R37NS037096/NINDS NIH HHS
  3. R21NS046669/NINDS NIH HHS

MeSH Term

Animals
Axons
Humans
Lectins, C-Type
Membrane Proteins
Models, Biological
Myelin-Associated Glycoprotein
Nerve Regeneration
Neuraminidase
Peripheral Nervous System Diseases

Chemicals

CHODL protein, human
Lectins, C-Type
Membrane Proteins
Myelin-Associated Glycoprotein
Neuraminidase

Word Cloud

Created with Highcharts 10.0.0nerveregenerationoutgrowthrecoveryARIsinhibitorsaxoninjuryglycoproteininhibitiontherebynervoussystemCNStraumaticAxonmyelin-associatedreceptorsmayspinalperipheralgraftsbrachialplexusavulsionfunctionalOBJECTIVE:increaseawarenessadvancementsMETHODS:ReviewliteratureregardingpresentationpotentialagentsreversepromotingRESULTS:injuredadultcentralinhibitslimitingcontributeincludeNogooligodendrocyte-myelinchondroitinsulfateproteoglycansbindspecificgrowthconehaltconsequentlyreversingblockingactionspromoteSialidaseenzymecleavesoneclassaxonalenhancesimplantedratmodelrootstorncordCONCLUSION:RepairusingpromisingrestorativesurgicaltreatmenthumansalthoughimprovementremainslimitedMoleculartherapiestargetingaidinjuriesdiseases

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