Horvat J C
Laboratoire de Neurobiologie, URA CNRS 1448, Université René Descartes, Paris.
Bull Acad Natl Med. 1994 Mar;178(3):455-63; discussion 464.
Spontaneous recovery from severe traumatic lesions of the central nervous system (CNS) does not occur in adult mammals for two main reasons: the lost neurons are not replaced and the surviving axotomized nerve cells do not regenerate the missing part of their cut axon, thus failing to reestablish the original anatomical and functional connections. The likeliest explanation for this lack of axonal regrowth is powerful inhibitory effects from mature reactive astrocytes and oligodendrocytes. However, experimental strategies making use of transplantation techniques have proved to be rather efficient. Thus, with regard to spinal cord injury: 1) lost spinal neurons (especially motoneurons) can, to some extent, be replaced by foetal spinal neurons transplanted to the lesion site; 2) irreversible damage to spinal projections from supraspinal neurons (mainly localized in the brain stem) can partially be compensated by grafting homologous foetal nerve cells caudally with regard to the spinal lesion site; 3) axogenesis from transplanted nerve cells or axonal regrowth from injured host neurons can be triggered and guided towards central or peripheral targets by autologous peripheral nerve segments which bypass the lesion site. This efficient cellular therapy is on the way to be complemented by a gene therapy that will allow the introduction, into the brain and the spinal cord, either of genetically modified cells from various origins, or of selected beneficial genes previously integrated into viral vectors.