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Curr Opin Neurobiol. 2014 Aug;27:53-60. doi: 10.1016/j.conb.2014.02.011. Epub 2014 Mar 12.

Nogo limits neural plasticity and recovery from injury.

Author information

1
Brain Research Institute, University of Zurich, Winterthurerstr.190, Zurich CH-8057, Switzerland. Electronic address: schwab@hifo.uzh.ch.
2
Department of Neurology, and Interdepartmental Program in Cellular Neuroscience, Neurodegeneration, and Repair (CNNR), Yale University School of Medicine, BCMM 436, 295 Congress Avenue, New Haven, CT 06510, USA. Electronic address: stephen.strittmatter@yale.edu.

Abstract

The expression of Nogo-A and the receptor NgR1 limits the recovery of adult mammals from central nervous system injury. Multiple studies have demonstrated efficacy from targeting this pathway for functional recovery and neural repair after spinal cord trauma, ischemic stroke, optic nerve injury and models of multiple sclerosis. Recent molecular studies have added S1PR2 as a receptor for the amino terminal domain of Nogo-A, and have demonstrated shared components for Nogo-A and CSPG signaling as well as novel Nogo antagonists. It has been recognized that neural repair involves plasticity, sprouting and regeneration. A physiologic role for Nogo-A and NgR1 has been documented in the restriction of experience-dependent plasticity with maturity, and the stability of synaptic, dendritic and axonal anatomy.

PMID:
24632308
PMCID:
PMC4122629
DOI:
10.1016/j.conb.2014.02.011
[Indexed for MEDLINE]
Free PMC Article

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