Forebrain neurogenesis after focal Ischemic and traumatic brain injury
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 s...
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| Format: | Article |
| Language: | English |
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Elsevier
2010-02-01
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| Series: | Neurobiology of Disease |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0969996109003131 |
| _version_ | 1819119485308633088 |
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| author | Steven G. Kernie Jack M. Parent |
| author_facet | Steven G. Kernie Jack M. Parent |
| author_sort | Steven G. Kernie |
| collection | DOAJ |
| description | 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 functional 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. |
| first_indexed | 2024-12-22T06:05:31Z |
| format | Article |
| id | doaj.art-26b85437080c46f780d7cd09a6c6cb57 |
| institution | Directory Open Access Journal |
| issn | 1095-953X |
| language | English |
| last_indexed | 2024-12-22T06:05:31Z |
| publishDate | 2010-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Neurobiology of Disease |
| spelling | doaj.art-26b85437080c46f780d7cd09a6c6cb572022-12-21T18:36:25ZengElsevierNeurobiology of Disease1095-953X2010-02-01372267274Forebrain neurogenesis after focal Ischemic and traumatic brain injurySteven G. Kernie0Jack M. Parent1Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA; Corresponding authors. S.G. Kernie is to be contacted at Department of Pediatrics, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd. ND5.124A, Dallas, TX 75390-9133, USA. Fax: +1 214 648 1960. J.M. Parent, Department of Neurology, University of Michigan Medical Center, 5021 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, USA. Fax: +1 734 763 7686.Department of Neurology, University of Michigan Medical Center, Ann Arbor, MI, USA; Corresponding authors. S.G. Kernie is to be contacted at Department of Pediatrics, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd. ND5.124A, Dallas, TX 75390-9133, USA. Fax: +1 214 648 1960. J.M. Parent, Department of Neurology, University of Michigan Medical Center, 5021 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, USA. Fax: +1 734 763 7686.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 functional 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.http://www.sciencedirect.com/science/article/pii/S0969996109003131 |
| spellingShingle | Steven G. Kernie Jack M. Parent Forebrain neurogenesis after focal Ischemic and traumatic brain injury Neurobiology of Disease |
| title | Forebrain neurogenesis after focal Ischemic and traumatic brain injury |
| title_full | Forebrain neurogenesis after focal Ischemic and traumatic brain injury |
| title_fullStr | Forebrain neurogenesis after focal Ischemic and traumatic brain injury |
| title_full_unstemmed | Forebrain neurogenesis after focal Ischemic and traumatic brain injury |
| title_short | Forebrain neurogenesis after focal Ischemic and traumatic brain injury |
| title_sort | forebrain neurogenesis after focal ischemic and traumatic brain injury |
| url | http://www.sciencedirect.com/science/article/pii/S0969996109003131 |
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