**3. Conclusions and comments**

There is a broad range of animal models that address distinct aspects of multiple sclerosis and other demyelinating diseases. Each of the models has specific strengths and weaknesses in furthering our understanding of the pathogenic processes that mediate demyelination and in identifying new opportunities for the effective promotion of myelin repair. EAE models have led to the development of many therapeutic targets aimed at halting disease progression. More recently, other models such as those targeting oligodendrocyte cell death have been instrumental in fine-tuning our understanding of the pathology of demyelination/ remyelination in MS and other similar diseases. Each of the model systems discussed in this review deserves particular credit, as it has helped solve a different piece of the puzzle. For example, while EAE models have unraveled many of the immunological bases of the CNS demyelination, particularly the role of T cells in MS, the use of glial toxins such as LPC or ethidium bromide has emerged as extremely useful in reshaping our understanding of the environmental and cell-based mechanisms of remyelination, and the models of oligodendrocyte death provide insights into factors driving the pathology. It seems likely that new models will be forthcoming that more effectively address the role of cells other than those of the immune and oligodendrocyte lineage. Understanding the role of microglia and astrocytes, as well as further clarity around the mechanism of vascular components in disease progression, will allow new therapeutic avenues to be developed in future studies.
