Deviating From the Well Travelled Path: Precursor Cell Migration in the Pathological Adult Mammalian Brain

Deviating From the Well Travelled Path: Precursor Cell Migration in the Pathological Adult Mammalian Brain
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DOI:
10.1002/jcb.23086
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发表时间:
2011-06-01
影响因子:
4
通讯作者:
Maucksch, Christof
Maucksch, Christof
中科院分区:
生物学2区
文献类型:
--
作者:
Connor, Bronwen;Gordon, Renee J.;Maucksch, Christof

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在成人中枢神经系统(CNS)中神经和神经胶质前体细胞的存在以及这些细胞通过该成熟结构迁移到病理损伤和损伤区域的能力为开发治疗脑损伤和疾病的新治疗策略带来了希望。虽然目前,在各种类型的脑病理学后描述的补偿性神经发生似乎是适度的,但促进内源性前体细胞向神经细胞损失区域的定向动员和表型诱导的策略的发展仍然具有很高的兴趣。然而,这种策略的发展目前受到对影响前体细胞迁移的过程和因素的有限理解的阻碍。在这篇综述中,我们将讨论目前的知识周围的前体细胞迁移的病理成人大脑,特别关注的反应和命运的前体亚群神经细胞的损失和炎症系统介导的前体细胞迁移的作用。通过这次讨论,我们将确定需要进一步详细研究的特定领域,以扩大我们目前的理解,并帮助最终开发一种新的治疗应用。J.细胞。112:1467-1474,2011。(C)2011 Wiley-Liss,Inc.
The presence of both neural and glial precursor cells in the adult central nervous system (CNS) and the capacity of these cells to migrate through this mature structure to areas of pathological damage and injury raises hope for the development of new therapeutic strategies to treat brain injury and disease. Although at present time, the compensatory neurogenesis described after various types of brain pathologies appears to be modest, the development of a strategy promoting the directed mobilization and phenotypic induction of endogenous precursor cells to areas of neural cell loss remains of high interest. The development of such a strategy however is currently thwarted by a limited understanding of the process and factors influencing precursor cell migration. In this review, we will discuss the current knowledge around precursor cell migration in the pathological adult brain with particular focus on the response and fate of precursor sub-populations to neural cell loss and the role of the inflammatory system in mediating precursor cell migration. Through this discussion we will identify particular areas in which further detailed research is required in order to expand our current understanding and aid in the eventual development of a novel therapeutic application. J. Cell. Biochem. 112: 1467-1474, 2011. (C) 2011 Wiley-Liss, Inc.