Potentials of endogenous neural stem cells in cortical repair

被引:43
作者
Saha, Bhaskar [1 ]
Jaber, Mohamed [1 ]
Gaillard, Afsaneh [1 ]
机构
[1] Univ Poitiers, Expt & Clin Neurosci Lab, Cellular Therapies Brain Dis Grp, INSERM,U1084, F-86022 Poitiers, France
关键词
subventricular zone; proliferation; migration; lesion; TRAUMATIC BRAIN-INJURY; BLOOD-VESSELS FORM; SUBVENTRICULAR ZONE; SONIC-HEDGEHOG; GROWTH-FACTOR; NEUROBLAST MIGRATION; NEURONAL REPLACEMENT; REACTIVE ASTROCYTES; DIRECTED MIGRATION; CHAIN-MIGRATION;
D O I
10.3389/fncel.2012.00014
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In the last few decades great thrust has been put in the area of regenerative neurobiology research to combat brain injuries and neurodegenerative diseases. The recent discovery of neurogenic niches in the adult brain has led researchers to study how to mobilize these cells to orchestrate an endogenous repair mechanism. The brain can minimize injury induced damage by means of an immediate glial response and by initiating repair mechanisms that involve the generation and mobilization of new neurons to the site of injury where they can integrate into the existing circuit. This review highlights the current status of research in this field. Here, we discuss the changes that take place in the neurogenic milieu following injury. We will focus, in particular, on the cellular and molecular controls that lead to increased proliferation in the Sub ventricular Zone (SVZ) as well as neurogenesis. We will also concentrate on how these cellular and molecular mechanisms influence the migration of new cells to the affected area and their differentiation into neuronal/glial lineage that initiate the repair mechanism. Next, we will discuss some of the different factors that limit/retard the repair process and highlight future lines of research that can help to overcome these limitations. A clear understanding of the underlying molecular mechanisms and physiological changes following brain damage and the subsequent endogenous repair should help us develop better strategies to repair damaged brains.
引用
收藏
页数:10
相关论文
共 131 条
  • [21] Cell migration in the normal and pathological postnatal mammalian brain
    Cayre, Myriam
    Canoll, Peter
    Goldman, James E.
    [J]. PROGRESS IN NEUROBIOLOGY, 2009, 88 (01) : 41 - 63
  • [22] Neurogenesis and glial proliferation persist for at least one year in the subventricular zone following brain trauma in rats
    Chen, XH
    Iwata, A
    Nonaka, M
    Browne, KD
    Smith, DH
    [J]. JOURNAL OF NEUROTRAUMA, 2003, 20 (07) : 623 - 631
  • [23] Astrocytes and brain injury
    Chen, YM
    Swanson, RA
    [J]. JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2003, 23 (02) : 137 - 149
  • [24] NGF, DCX, and NSE upregulation correlates with severity and outcome of head trauma in children
    Chiaretti, A.
    Barone, G.
    Riccardi, R.
    Antonelli, A.
    Pezzotti, P.
    Genovese, O.
    Tortorolo, L.
    Conti, G.
    [J]. NEUROLOGY, 2009, 72 (07) : 609 - 616
  • [25] Traumatic brain injury induced cell proliferation in the adult mammalian central nervous system
    Chirumamilla, S
    Sun, D
    Bullock, MR
    Colello, RJ
    [J]. JOURNAL OF NEUROTRAUMA, 2002, 19 (06) : 693 - 703
  • [26] Dopamine D3 receptor stimulation promotes the proliferation of cells derived from the post-natal subventricular zone
    Coronas, V
    Bantubungi, K
    Fombonne, J
    Krantic, S
    Schiffmann, SN
    Roger, M
    [J]. JOURNAL OF NEUROCHEMISTRY, 2004, 91 (06) : 1292 - 1301
  • [27] Courtès S, 2011, PLOS ONE, V6, DOI 10.1371/journal.pone.0020430
  • [28] Defining the Critical Period for Neocortical Neurogenesis after Pediatric Brain Injury
    Covey, Matthew V.
    Jiang, Yuhui
    Alli, Vamsi V.
    Yang, Zhengang
    Levison, Steven W.
    [J]. DEVELOPMENTAL NEUROSCIENCE, 2010, 32 (5-6) : 488 - 498
  • [29] A PROTEIN RELATED TO EXTRACELLULAR-MATRIX PROTEINS DELETED IN THE MOUSE MUTANT REELER
    DARCANGELO, G
    MIAO, GG
    CHEN, SC
    SOARES, HD
    MORGAN, JI
    CURRAN, T
    [J]. NATURE, 1995, 374 (6524) : 719 - 723
  • [30] Dash PK, 2001, J NEUROSCI RES, V63, P313, DOI 10.1002/1097-4547(20010215)63:4<313::AID-JNR1025>3.0.CO