Neurotherapeutics, 2011 · DOI: 10.1007/s13311-011-0033-5 · Published: April 1, 2011
After a spinal cord injury, oligodendrocytes, which are essential for insulating nerve fibers, are highly vulnerable and die off, leading to demyelination. This loss impairs the function and survival of axons, the long threads that carry nerve signals. In response to this damage, the body attempts to repair itself by generating new oligodendrocyte progenitor cells, especially around the injury site. These cells can mature into oligodendrocytes and begin to remyelinate damaged axons, typically starting about two weeks after the injury. The review analyzes mechanisms of oligodendrocyte loss and replacement, and myelination after SCI, highlighting areas for potential therapeutic intervention. It further discusses studies focused on protecting existing oligodendrocytes and replacing lost ones through growth factors and cell transplantation.
Identifying mechanisms of OL loss and replacement provides targets for therapeutic interventions after SCI.
Growth factors can boost the endogenous progenitor response and facilitate survival and OL fate in conjunction with progenitor transplantation.
Embryonic stem cell-derived cells and adult neural progenitor cells have shown considerable progress in OL protection and replacement.