Humoral response to John Cunningham virus during pregnancy in multiple sclerosis

ConclusionsJCV-Ab levels remain unaltered during MS pregnancy, while the total IgG concentration is reduced/diluted due to increasing plasma volumes during the course of pregnancy. This may imply a biologically significant alteration in the immune response to JCV during MS pregnancy.</p

Effect of the Sera of Patients with Multiple Sclerosis on Apoptosis and Nitric Oxide Production of Endothelial Cells

Abstract: Background & Aims: Multiple sclerosis (MS) is one of the chronic autoimmune diseases of the central nervous system with unknown etiology. The present study aimed to investigate the apoptosis and nitric oxide (NO) production of endothelial cells treated with serum of patients with MS and response to interferon beta (IFN-?) therapy. Methods: Human umbilical vein endothelial cells were treated with sera from patients with active MS (in relapse), MS in remission, or sera from healthy volunteers (each n = 10). Nitric oxide (NO) levels were determined in culture supernatants by Greiss method and endothelial cell apoptosis was assessed by annexin V-propidium iodide staining. Effects of IFN-beta-1b on endothelial cell apoptosis and NO production were tested at increasing doses (10, 100, and 1000 U/ml). Results: Compared with healthy people, only apoptosis of endothelial cells treated with serum of patients with relapsing phase increased, P<0.01; while there was no significant difference between apoptosis of endothelial cells treated with serum of patients in remission phase and healthy controls. Apoptosis of endothelial cells treated with sera of patients in relapse was decreased by IFN-beta-1b at 10 U/ml, P<0.05. The same dose also led to a significant increase in nitric oxide production. Conclusion: The results suggest that endothelial cells injury and apoptosis may play a role in MS etiology and represents a potential therapeutic mechanism of action for IFN-beta-1b in MS therapy. Keywords: Multiple sclerosis, Interferon beta-1b (IFN-beta-1b), Endothelial cell apoptosis, Nitric oxid

Dalfampridine: Review of its Efficacy in Improving Gait in Patients with Multiple Sclerosis

Multiple sclerosis (MS) is a progressive immune-mediated neurodegenerative disease of human central nervous system (CNS), which causes irreversible disability in young adults. The cause and cure for MS remain unknown. Pathophysiology of MS includes two arms: inflammatory demyelination and neurodegeneration. The inflammatory demyelination of MS which is mainly promoted by a massive activation of the immune system against putative CNS antigen(s) leads to loss of oligodendrocyte/myelin complex which slows down or halts impulse conduction in denuded axons. Practically, loss of myelin significantly reduces signal conduction along the demyelinated axons through alterations in the distribution of axonal ion channels. Dalfampridine (4-aminopyridine or 4-AP) is an oral potassium channel blocker, which was recently approved by FDA for symptomatic treatment of MS. Dalfampridine, which acts at the central and peripheral nervous systems, enhances conduction in demyelinated axons and improves walking ability of MS patients. A number of clinical trials have evaluated the safety and efficacy of fampridine in MS patients with the degree of gait improvement as the main outcome. The objective of this manuscript is to provide an overview of the pharmacology, pharmacokinetics, clinical trials, side effects and interactions of dalfampridine used in treatment of MS patients