Remyelinating and neuroprotective treatments in multiple sclerosis

Multiple sclerosis (MS) is the most common cause of neurological disability in young adults. The pathological hallmark is multifocal demyelination and inflammation in the CNS. In addition, there is also a variable extent of axonal damage. Remyelination has been seen in up to 70% of lesions but repair is generally incomplete. The demonstration of neuropathological heterogeneity of MS lesions suggests different pathophysiological subtypes and it is therefore unlikely that there is a uniform cause of incomplete remyelination in MS. In recent years, a great body of knowledge has accumulated in order to better understand the regulatory mechanisms of remyelination. This has led to a number of approaches to promote repair mechanisms, most of which have been successful in animal experiments. Unfortunately, the translation of these experimental data into clinical treatments has proven difficult. More information on the pathogenesis of MS, the reason why repair mechanisms fail in MS and a better understanding of the regulation of remyelination are required. This will ultimately lead to a specific treatment tailored for the individual patient and will probably involve a combination of immunomodulation, remyelination and neuroprotection.