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Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). The prevalence of MS is approximately 2 million people worldwide, with an incidence of about 1:1000 in Europe and Northern America, and women are affected more often compared to men, at a ratio of approximately 2:1. It is the most common cause of neurological disability among young adults with an onset generally between 20 and 40 years of age [Pugliatti et al., 2002]. The major neuropathological hallmarks of MS are demyelinating lesions associated with perivascular infiltrates, consisting of macrophages/microglia and lymphocytes. The lesions are characterized by destruction of myelin sheaths, oligodendrocyte death, axonal damage and glial scar formation, called astrogliosis. Demyelination is a central event in MS pathology. Although some remyelination occurs, it ultimately fails [Franklin, 2002]. The cause of the remyelination failure is not clear, although several processes have been suggested to play a role [Franklin and Ffrench-Constant, 2008; Wolswijk, 2002; John et al., 2002]. Not only processes behind remyelination failure remain elusive, also the cellular mechanisms behind the demyelination and axonal damage are largely unknown. Modelling MS both in animals and in vitro could help with understanding this. This chapter will focus on MS pathology and the models that exist for investigating this disease, especially zooming in on in vitro models.

Modelling Multiple Sclerosis In Vitro and the Influence of Activated Macrophages