Oligodendrocyte Reaction to Axonal Damage

Abstract

Most experimental and clinical studies of remyelination have in the past concentrated on the mechanism of formation of the myelin sheath and the behaviour of the oligodendrocyte (Ludwin 1987). It has become clear, that this process is composed of a variety of important steps, the understanding of each of which is essential in any future attempts to influence the possible extent of remyelination both experimentally and hopefully clinically. Attempts to enhance this remyelination potential are of importance not only in demyelinating diseases affecting mainly myelin and oligodendrocytes, but will increasingly assume importance in destructive diseases of the brain. With greater success in stimulating regeneration of axons and neurons in these situations,there will be a need for remyelination of these newly formed nerve processes. The importance of the oligodendrocyte has been well documented (Ludwin 1988, 1989), and it has been well emphasised that successful remyelination depends on an adequate number of oligodendrocytes, which may be provided by maturation of immature cells, possibly by proliferation of mature oligodendrocytes (Ludwin 1985, 1988), and more recently through the provision of exogenous oligodendrocytes to demyelinated areas (Blakemore & Crang, 1988). Those disease processes in which oligodendrocyte numbers remain high tend to have more successful remyelination, whereas diseases in which continual exposure to the demyelinating agent decreases the number of oligodendrocytes tend to have less successful remyelination (Ludwin 1987, Raine et al 1988).