Remyelination in experimental models of toxin-induced demyelination

Abstract

Remyelination is the regenerative process by which demyelinated axons are reinvested with new myelin sheaths. It is associated with functional recovery and maintenance of axonal health. It occurs as a spontaneous regenerative response following demyelination in a range of pathologies including traumatic injury as well as primary demyelinating disease such as multiple sclerosis (MS). Experimental models of demyelination based on the use of toxins, while not attempting to accurately mimic a disease with complex etiology and pathogenesis such as MS, have nevertheless proven extremely useful for studying the biology of remyelination. In this chapter, we review the main toxin models of demyelination, drawing attention to their differences and how they can be used to study different aspects of remyelination. We also describe the optimal use of these models, highlighting potential pitfalls in interpretation, and how remyelination can be unequivocally recognized. Finally, we discuss the role of toxin models alongside viral and immune-mediated models of demyelination.