Molecular targets in spinal cord injury

被引:41
作者
Klussmann, S [1 ]
Martin-Villalba, A [1 ]
机构
[1] German Canc Res Ctr, Div Immunogenet, Tumorimmunol Program, D-6900 Heidelberg, Germany
来源
JOURNAL OF MOLECULAR MEDICINE-JMM | 2005年 / 83卷 / 09期
关键词
Spinal trauma; Neuroprotective strategies; Molecular targets; Apoptosis; Myelin; Concomitant function;
D O I
10.1007/s00109-005-0663-3
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The spinal cord can be compared to a highway connecting the brain with the different body levels lying underneath, with the axons being the ultimate carriers of the electrical impulse. After spinal cord injury (SCI), many cells are lost because of the injury. To reconstitute function, damaged axons from surviving neurons have to grow through the lesion site to their initial targets. However, the territory they have to traverse has changed: the highway is full of inhibitory signals (myelin and scar components); the pavement itself has become bumpy (demyelination); and specialized cells are recruited to clear the way (inflammatory cells). Thus, actual strategies to treat spinal injuries aim at providing a permissive environment for regenerating axons and boosting the endogenous potential of axons to regenerate while limiting progression of secondary damage. Here we review some of the strategies currently under consideration to treat spinal injuries.
引用
收藏
页码:657 / 671
页数:15
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