Forebrain neurogenesis after focal Ischemic and traumatic brain injury.
Forebrain neurogenesis after focal Ischemic and traumatic brain injury.
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DOI：
10.1016/j.nbd.2009.11.002
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发表时间：
2010-02
影响因子：
6.1
通讯作者：
Parent JM
中科院分区：
文献类型：
--
作者：
Kernie SG;Parent JM
神经干细胞存在于成年哺乳动物的前脑中，是脑损伤后修复神经元的潜在来源。持续性神经发生的两个主要区域，脑室下区(SVZ)-嗅球通路和海马齿状回，受到大脑损伤(如中风或创伤)的刺激。在本实验中，我们重点研究了局灶性脑缺血对实验性卒中SVZ神经前体细胞的影响，以及机械损伤对创伤性脑损伤模型成年大鼠海马神经发生的影响。中风可以有效地刺激前脑SVZ细胞的增殖和神经发生。SVZ神经母细胞被诱导迁移到受损的纹状体，并在较小程度上迁移到梗塞周围皮质。关于损伤的纹状体中产生的神经元的类型以及成年出生的神经元是否有助于功能恢复仍存在争议。在了解SVZ神经发生的一般调控方面的进展，特别是在中风诱导的神经发生方面的进展，可能会改善成年出生的神经元在损伤部位的整合和存活。实验性颅脑损伤后，齿状回细胞增殖和神经发生类似地增加。然而，齿状回中原有的神经母细胞很容易受到创伤的伤害，这似乎会刺激SGZ中的神经干细胞增殖并取代它们，导致新的颗粒细胞数量增加。刺激海马神经发生的干预措施似乎能改善实验性脑损伤后的认知恢复。有条件地标记或去除神经干细胞的转基因方法开始进一步解决有关中风或脑外伤后神经发生的潜在机制和功能意义的关键问题。未来的治疗目标应该是在缺血性或创伤性损伤后指导适当的神经元替代，同时抑制可能导致癫痫或认知障碍等共病的异常整合。
Neural stem cells persist in the adult mammalian forebrain and are a potential source of neurons for repair after brain injury. The two main areas of persistent neurogenesis, the subventricular zone (SVZ)-olfactory bulb pathway and hippocampal dentate gyrus, are stimulated by brain insults such as stroke or trauma. Here we focus on the effects of focal cerebral ischemia on SVZ neural progenitor cells in experimental stroke, and the influence of mechanical injury on adult hippocampal neurogenesis in models of traumatic brain injury (TBI). Stroke potently stimulates forebrain SVZ cell proliferation and neurogenesis. SVZ neuroblasts are induced to migrate to the injured striatum, and to a lesser extent to the peri-infarct cortex. Controversy exists as to the types of neurons that are generated in the injured striatum, and whether adult-born neurons contribute to functional restoration remains uncertain. Advances in understanding the regulation of SVZ neurogenesis in general, and stroke-induced neurogenesis in particular, may lead to improved integration and survival of adult-born neurons at sites of injury. Dentate gyrus cell proliferation and neurogenesis similarly increase after experimental TBI. However, pre-existing neuroblasts in the dentate gyrus are vulnerable to traumatic insults, which appear to stimulate neural stem cells in the SGZ to proliferate and replace them, leading to increased numbers of new granule cells. Interventions that stimulate hippocampal neurogenesis appear to improve cognitive recovery after experimental TBI. Transgenic methods to conditionally label or ablate neural stem cells are beginning to further address critical questions regarding underlying mechanisms and function significance of neurogenesis after stroke or TBI. Future therapies should be aimed at directing appropriate neuronal replacement after ischemic or traumatic injury while suppressing aberrant integration that may contribute to co-morbidities such as epilepsy or cognitive impairment.
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影响因子：
82.9
作者：
Eriksson, PS;Perfilieva, E;Gage, FH
通讯作者：
Gage, FH
DOI：
10.1073/pnas.0601992103
发表时间：
2006-05-23
影响因子：
11.1
作者：
Encinas, Juan M.;Vaahtokari, Anne;Enikolopov, Grigori
通讯作者：
Enikolopov, Grigori
影响因子：
2.5
作者：
COROTTO, FS;HENEGAR, JA;MARUNIAK, JA
通讯作者：
MARUNIAK, JA
影响因子：
25
作者：
Denise, A;Garcia, R;Sofroniew, MV
通讯作者：
Sofroniew, MV
影响因子：
5.6
作者：
Diaz-Arrastia, Ramon;Agostini, Mark A.;Van Ness, Paul C.
通讯作者：
Van Ness, Paul C.