FAILURE TO ACHIEVE REMYELINATION OF DEMYELINATED RAT AXONS FOLLOWING TRANSPLANTATION OF GLIAL-CELLS OBTAINED FROM THE ADULT HUMAN BRAIN

Citation
Mp. Targett et al., FAILURE TO ACHIEVE REMYELINATION OF DEMYELINATED RAT AXONS FOLLOWING TRANSPLANTATION OF GLIAL-CELLS OBTAINED FROM THE ADULT HUMAN BRAIN, Neuropathology and applied neurobiology, 22(3), 1996, pp. 199-206
Citations number
35
Categorie Soggetti
Neurosciences,"Clinical Neurology",Pathology
ISSN journal
03051846
Volume
22
Issue
3
Year of publication
1996
Pages
199 - 206
Database
ISI
SICI code
0305-1846(1996)22:3<199:FTAROD>2.0.ZU;2-N
Abstract
The ability of transplanted glial cells to myelinate axons in experime ntal animals offers the prospect that it may be possible to achieve re myelination in human demyelinating disease by the implantation of olig odendrocyte lineage cells. Autologous normal white matter could repres ent a potential source of cells whose use would avoid tissue rejection and overcome ethical and practical constraints associated with the us e of fetal tissue. To determine the remyelinating potential of cells i solated from adult human CNS, a cell preparation prepared from adult h uman white matter which contained 56% oligodendrocytes, 3% preoligoden drocytes and 1% precursor cells was transplanted into non-repairing de myelinating lesions in immunosuppressed rats created by the injection of ethidium bromide into x-irradiated spinal cord white matter, The ex tent of remyelination was examined 3 and 5 weeks after transplantation , Although the transplanted oligodendrocytes survived in the area of d emyelination, associated with demyelinated axons and produced myelin m embranes, no myelin sheaths were produced and there was no evidence of cell migration or division, The failure of human oligodendrocytes to form myelin sheaths may reflect the poor remyelinating potential of po st mitotic oligodendrocytes, and the failure of the small number of co -transplanted bipotential oligodendrocyte progenitor cells to differen tiate and myelinate axons may be a consequence of lack of appropriate environmental factors within the rat lesion required for expansion and differentiation of these cells.