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Nogo limits neural plasticity and recovery from injury
Author(s):
Martin E Schwab
,
Stephen M Strittmatter
Publication date
Created:
August 2014
Publication date
(Print):
August 2014
Journal:
Current Opinion in Neurobiology
Publisher:
Elsevier BV
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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. Copyright © 2014 Elsevier Ltd. All rights reserved.
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Journal
Title:
Current Opinion in Neurobiology
Abbreviated Title:
Current Opinion in Neurobiology
Publisher:
Elsevier BV
ISSN (Print):
09594388
Publication date Created:
August 2014
Publication date (Print):
August 2014
Volume
: 27
Pages
: 53-60
Article
DOI:
10.1016/j.conb.2014.02.011
PMC ID:
4122629
PubMed ID:
24632308
SO-VID:
c756488f-796e-4201-a4d4-db9858494828
Copyright ©
© 2014
License:
https://www.elsevier.com/tdm/userlicense/1.0/
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