Disease-modifying therapy in multiple sclerosis and chronic inflammatory demyelinating polyradiculoneuropathy: common and divergent current and future strategies

Abstract

OTHER ARTICLES PUBLISHED IN THIS SERIESParaneoplastic neurological syndromes. Clinical and Experimental Immunology 2014, 175: 336-48. Diagnosis, pathogenesis and treatment of myositis: recent advances. Clinical and Experimental Immunology 2014, 175: 349-58. Monoclonal antibodies in treatment of multiple sclerosis. Clinical and Experimental Immunology 2014, 175: 373-84 SummaryMultiple sclerosis (MS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) represent chronic, autoimmune demyelinating disorders of the central and peripheral nervous system. Although both disorders share some fundamental pathogenic elements, treatments do not provide uniform effects across both disorders. We aim at providing an overview of current and future disease-modifying strategies in these disorders to demonstrate communalities and distinctions.

Untargeted Plasma Metabolomics Identifies Endogenous Metabolite with Drug-like Properties in Chronic Animal Model of Multiple Sclerosis

“…Most of the Food and Drug Administration-approved MS therapies including, interferon ␤, glatiramer acetate, dimethyl fumarate, laquinimod, and fingolimod, are anti-inflammatory in action (82,83). Glatiramer acetate and laquinimod have been shown to induce type II monocytes and reverse the EAE disease by modulating T cell response (49,84).…”

Targeting B cells in relapsing–remitting multiple sclerosis: from pathophysiology to optimal clinical management

“…Alongside the variety of indications, there are many different dosing and application strategies. In MS rituximab is commonly administered intravenously either at a dose of 1000 mg on days 1 and 15, or 375 mg/m 2 in 4-weekly doses every 6-12 months [Kim et al 2013;Melzer and Meuth, 2014]. Concomitant steroids, antihistaminic and antipyretic drugs are used to reduce infusion-associated adverse reactions.…”

A brief glimpse over the horizon for type 1 diabetes nanotherapeutics

“…Allergies including allergic asthma and severe food allergies affect~20% of the population while the prevalence of autoimmune diseases in the general population is currently at 4.5% [11][12][13][14][15][16][17]. The standard-of-care as well as emerging therapies are centered on systemic delivery of immunosuppresive drugs that require chronic administration which can exacerbate opportunistic infections, reactivate latent pathogens and can predispose to malignancy [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33]. Emerging data indicate that other than targeting the specific effector cells involved in the actual tissue damage, it may be more attractive and easier, to target a therapeutic to the site(s) where immune cells acquire the ability to become effector cells (those that actually physically cause the damage, either by cytokines or by direct killing).…”