Remyelination in animal models of multiple sclerosis: finding the elusive grail of regeneration

Remyelination biology and the therapeutic potential of restoring myelin sheaths to prevent neurodegeneration and disability in multiple sclerosis (MS) has made considerable gains over the past decade with many regeneration strategies undergoing tested in MS clinical trials. Animal models used to investigate oligodendroglial responses and regeneration of myelin vary considerably in the mechanism of demyelination, involvement of inflammatory cells, neurodegeneration and capacity for remyelination. The investigation of remyelination in the context of aging and an inflammatory environment are of considerable interest for the potential translation to progressive multiple sclerosis. Here we review how remyelination is assessed in mouse models of demyelination, differences and advantages of these models, therapeutic strategies that have emerged and current pro-remyelination clinical trials.

Automated summary

Significant progress has been made in understanding the biology of remyelination and its potential as a therapeutic strategy for preventing neurodegeneration and disability in multiple sclerosis (MS). Different animal models have been used to study oligodendroglial responses and remyelination, each with its own mechanisms of demyelination, involvement of inflammatory cells, neurodegeneration, and capacity for remyelination. It is important to investigate remyelination in the context of aging and an inflammatory environment for potential translation to progressive MS. This review discusses the assessment of remyelination in mouse models of demyelination, the differences and advantages of these models, emerging therapeutic strategies, and current clinical trials promoting remyelination.