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脑损伤后神经可塑性的机制。

Mechanisms of neural plasticity following brain injury.

作者信息

Wieloch Tadeusz, Nikolich Karoly

机构信息

Laboratory for Experimental Brain Research, Wallenberg Neuroscience Center, University of Lund, BMCA13, 221 85 Lund, Sweden.

出版信息

Curr Opin Neurobiol. 2006 Jun;16(3):258-64. doi: 10.1016/j.conb.2006.05.011. Epub 2006 May 18.

DOI:10.1016/j.conb.2006.05.011
PMID:16713245
Abstract

Brain insults cause rapid cell death, and a disruption of functional circuits, in the affected regions. As the injured tissue recovers from events associated with cell death, regenerative processes are activated that over months lead to a certain degree of functional recovery. Factors produced by new neurons and glia, axonal sprouting of surviving neurons, and new synapse formation help to re-establish some of the lost functions. The timing and location of such events is crucial in the success of the regenerative process. Comprehensive gene expression profiling and proteomic analyses have enabled a deeper molecular and cellular mechanistic understanding of post-injury brain regeneration. These new mechanistic insights are aiding the design of novel therapeutic modalities that enhance regeneration.

摘要

脑损伤会导致受影响区域的细胞迅速死亡以及功能回路中断。随着受损组织从与细胞死亡相关的事件中恢复,再生过程被激活,在数月内会导致一定程度的功能恢复。新神经元和神经胶质细胞产生的因子、存活神经元的轴突发芽以及新突触的形成有助于重新建立一些丧失的功能。这些事件的时间和位置对于再生过程的成功至关重要。全面的基因表达谱分析和蛋白质组学分析已使人们能够更深入地从分子和细胞机制层面理解损伤后脑的再生。这些新的机制见解有助于设计促进再生的新型治疗方法。

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