Nogo limits neural plasticity and recovery from injury.

Nogo limits neural plasticity and recovery from injury.
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DOI:
10.1016/j.conb.2014.02.011
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发表时间:
2014-08
影响因子:
5.7
通讯作者:
Strittmatter SM
Strittmatter SM
中科院分区:
医学2区
文献类型:
--
作者:
Schwab ME;Strittmatter SM

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Nogo-A和受体NgR 1的表达限制了成年哺乳动物从中枢神经系统损伤中的恢复。多项研究已经证明了靶向这一途径对脊髓创伤、缺血性中风、视神经损伤和多发性硬化模型后的功能恢复和神经修复的疗效。最近的分子研究增加了S1 PR 2作为Nogo-A的氨基末端结构域的受体,并且已经证明了Nogo-A和CSPG信号传导的共享组分以及新的Nogo拮抗剂。神经修复涉及可塑性、发芽和再生。Nogo-A和NgR 1的生理作用已被证明是限制经验依赖性可塑性与成熟,和稳定的突触,树突和轴突解剖。
The expression of Nogo-A and the receptor NgR1 limit 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 signalling 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.
抗Nogo-A抗体治疗促进成年灵长类单侧颈椎损伤后手灵巧度的恢复——行为数据的重新检查和扩展。
DOI: 10.1111/j.1460-9568.2009.06642.x
发表时间: 2009-03
期刊: The European journal of neuroscience
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