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Monday, November 12, 2012

Long-term Experience of Glatiramer Acetate (Copaxone®) in the Treatment of Clinically Isolated Syndrome and Relapsing–Remitting Multiple Sclerosis

November 2012

By: Howard Zwibel

As a chronic disease of the central nervous system (CNS), multiple sclerosis (MS) is characterized by a complex interplay between inflammation, demyelination, remyelination, gliosis, and neuronal injury.1 it continues to be a major cause of acquired neurologic disability in young adults worldwide, particularly in people of northern european origin.2 it affects women with twice the frequency of men and the average age of diagnosis is 37 years.3 The worldwide total estimated prevalence for the past three decades is 83 cases/100,000 population.4

The clinical course of MS is heterogeneous, with variability both between and within patients, and has been categorized as clinically isolated syndrome (CIS), relapsing–remitting MS (RRMS, which accounts for 85 % of MS patients in the initial disease course), primary progressive MS (PPMs), and secondary progressive MS (SPMS).5,6 RRMS is characterized by relapses, symptoms of which include numbness, blurred vision, difficulty walking, fatigue, and pain. symptoms are usually temporary and are followed by periods of remission.6

The immunopathogenesis of MS is thought to be heterogeneous; however, the inflammatory demyelinating plaque is characteristic of all forms of MS.7 immune-mediated injury to myelin and oligodendrocytes may occur when peptides in myelin attach to the cleft of major histocompatibility complex (MHC) class ii molecules on antigen-presenting cells (APCS) including macrophages, monocytes, and dendritic cells.8 Activation of APcs can trigger an immune response against the bound antigen and leads to secretion of pro-inflammatory cytokines and the differentiation of naive cD4+ T cells into T-helper 1 (Th1) and T-helper 17 (Th17) cells, resulting in inflammation and autoimmunity. Th1 and Th17 cells are capable of migration into the cns and have been identified in active lesions.9,10 Th1 cells undergo continued proliferation and secretion of pro-inflammatory cytokines, leading to myelin damage and neuronal loss. further activation of resident microglia can lead to cross-reactivity, which maintains inflammation and further damage to the myelin sheath.11 impaired function of regulatory T cells (Tregs), which act against autoimmunity, allows further pathologic activation of autoreactive T cells and exacerbates the feedback loop that causes continual damage to the cns.12 Additionally, activated B cells appear to be participants in the creation of myelin lesions by producing antibodies that mediate and promote demyelination.13

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