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Pharmacogenomics in Multiple Sclerosis

Manuel Comabella, MD and Xavier Montalban, MD

Multiple sclerosis (MS) is a chronic T cell-mediated autoimmune inflammatory disease of the central nervous system (CNS) that leads to significant neurological disability, particularly in young people. MS is pathologically characterized by autoimmune inflammation, demyelination, axonal damage, and gliosis. To date, the etiology of MS is largely unknown; however, complex genetics and environmental triggers such as viral infections are thought to contribute to disease manifestation [1]. MS is heterogeneous in clinical course and disease severity (relapse-onset versus primary progressive forms, benign versus severe evolution), in brain magnetic resonance imaging (MRI) findings (inflammation versus atrophy) [2,3], in histopathological characteristics of brain lesions (cell-mediated versus antibody-mediated) [4], and in response to treatment [5,6]. With respect to treatment response, some MS patients experience an important reduction in the number of brain lesions and clinical exacerbations and show a lack of disease progression upon receiving therapy. These patients are considered “responders”. In contrast, other patients continue to suffer relapses and progression of the disease in spite of treatment, and are classified as “non-responders”. Although the mechanisms underlying this heterogeneity in treatment response are not completely understood, genetic factors are likely to play an important role. This provides rationale for the use of pharmacogenomics to try and identify those patients who will respond (or who will not respond) to a particular therapy.

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