Traumatic injury to the brain or spinal cord and multiple sclerosis (MS) share a common pathophysiology with regard to axonal demyelination. Despite advances in central nervous system (CNS) repair in experimental animal models, adequate functional recovery has yet to be achieved in patients in response to any of the current strategies. Functional recovery is dependent, in large part, upon remyelination of spared or regenerating axons. The mammalian CNS maintains an endogenous reservoir of glial precursor cells (GPCs), capable of generating new oligodendrocytes and astrocytes. These GPCs are upregulated following traumatic or demyelinating lesions, followed by their differentiation into oligodendrocytes. However, this innate response does not adequately promote remyelination. As a result, researchers have been focusing their efforts on harvesting, culturing, characterizing, and transplanting GPCs into injured regions of the adult mammalian CNS in a variety of animal models of CNS trauma or demyelinating disease. The technical and logistic considerations for transplanting GPCs are extensive and crucial for optimizing and maintaining cell survival before and after transplantation, promoting myelination, and tracking the fate of transplanted cells. This is especially true in trials of GPC transplantation in combination with other strategies such as neutralization of inhibitors to axonal regeneration or remyelination. Overall, such studies improve our understanding and approach to developing clinically relevant therapies for axonal remyelination following traumatic brain injury (TBI) or spinal cord injury (SCI) and demyelinating diseases such as MS.
|Original language||English (US)|
|Number of pages||54|
|Journal||Progress in Histochemistry and Cytochemistry|
|State||Published - Sep 10 2008|
Bibliographical noteFunding Information:
Funding for this work was provided by grants from the Ontario Neurotrauma Foundation, Canadian Paraplegic Association (Ontario Branch), Physician's Services Incorporated, and the Christopher Reeve Paralysis Foundation (C.H. Tator). Personal support was provided by an Ontario Student Opportunity Trust Fund/Vision Sciences Scholarship and Sandra and David Smith Graduate Student Award (I. Kulbatski), Canadian Institutes of Health Research Fellowships (A.J. Mothe, A.M. Parr), Ontario Neurotrauma Foundation Fellowships (A.J. Mothe, H. Kim, C.E. Kang), a Natural Sciences and Engineering Research Council of Canada Fellowship (H. Kim), and a Turkish Neurosurgical Society Fellowship (G. Bozkurt). We extend our appreciation to all these organizations for their support.