Towards individualised multiple-sclerosis therapy

摘要

More than 160 years after the first systematic description of multiple sclerosis (MS), our therapeutic tools for stopping disease progression are still limited, and there is not even a cure, let alone a way of repairing damage to the nervous system. A major reason for limited treatment options for MS is disease heterogeneity. MS can present with relapses and remissions or steady progression of neurological disability, meaning the disease course is unpredictable in each patient. The pathological hallmark in patients with acute and relapsing disease is the formation of focal inflammatory demyelinating lesions in white matter.1 Studies at the cellular and molecular levels led to the classification of actively demyelinating MS plaques into distinct pathological patterns I-IV of MS.2 More than 80% of analysed lesions are pattern I with cellular cytotoxicity or pattern II with antibody and complement mediated demyelination. As yet there is no unequivocal surrogate marker that is indicative of or associated with these lesion patterns.