AffiliationDepartment of Neurology, St. Vincent's University Hospital, Dublin, Ireland., firstname.lastname@example.org
MeSHAntibodies, Monoclonal/*therapeutic use
Antibodies, Monoclonal, Humanized
Multiple Sclerosis/*drug therapy/immunology
MetadataShow full item record
CitationJ Interferon Cytokine Res. 2010 Oct;30(10):787-9.
JournalJournal of interferon & cytokine research : the official journal of the, International Society for Interferon and Cytokine Research
AbstractMultiple sclerosis (MS) is the commonest disabling neurological disease of young and middle-aged adults affecting 1 million persons world wide. The illness begins with a relapsing-remitting MS course in 85%-90% of patients; the other 10%-15% have a primary progressive onset MS. Our current understanding is that MS is an autoimmune disorder with an inflammatory T-cell attack on myelin or some component of the oligodendrocyte--myelin structure. Relapses of disease activity result in plaques of demyelination with destruction of myelin and, to a lesser, extent axons. Lymphocytes within the central nervous system tissue recruit more cells leading to an inflammatory cascade that causes myelin damage, axonal disruption, and neuronal death. If the plaque occurs in a vocal area of the central nervous system then symptoms relating to that area result. However, magnetic resonance imaging shows that approximately 10 times more lesions occur in asymptomatic areas of the brain. Recovery from an initial relapse may appear relatively complete but persistent inflammation results in axonal injury and residual disability results. With time and accumulated lesion load, secondary degeneration of denuded axons results in the phase of secondary progressive MS usually 15-20 years after onset.