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Current Nanoscience

Editor-in-Chief

ISSN (Print): 1573-4137
ISSN (Online): 1875-6786

Etiopathogenesis, Classical Immunotherapy and Innovative Nanotherapeutics for Inflammatory Neurological Disorders

Author(s): Maria Jose Sa, Joana Guimaraes, Pedro Abreu, Amelia Mendes and Eliana B. Souto

Volume 7, Issue 1, 2011

Page: [2 - 20] Pages: 19

DOI: 10.2174/157341311794480318

Price: $65

Abstract

Central nervous system (CNS) inflammation and neurological diseases are clinical conditions requiring a multifaceted spectrum of immunotherapies. The present paper reviews the etiopathogeny of demyelinating diseases located in the CNS (e.g., multiple sclerosis, acute disseminated encephalomyelitis, and neuromyelitis optica), and in the peripheral nervous system (e.g., acute/chronic idiophathic inflammatory polyradiculoneuritis, and other dysimmune neuropathies). The pharmacological treatments here discussed include non-specific strategies (e.g., glucocorticoids, intravenous immunoglobulin) and others more specific, such as human IFNβ, glatiramer acetate, mitoxantrone, monoclonal antibodies, fingolimod, laquinimod, cladribine, fumarate, teriflunomide. The immunotherapies are described in terms of their specific and/or multiple activity in the disease stage of development (i.e., initiation, central/peripheral activation, molecular stimulation and immune effector responses during early, transitional and late phases). In the light of the current pharmacological treatments, novel site specific approaches using nanoparticles are briefly addressed.

Keywords: Nervous system inflammation, demyelinating diseases, multiple sclerosis, immunotherapeutics, nanotherapeutics, Etiopathogenesis, Inflammatory Neurological Disorders, Central nervous system, polyradiculoneuritis, glatiramer, mitoxantrone, monoclonal antibodies, fingolimod, laquinimod, cladribine, fumarate, teriflunomide, encephalomyelitis (EAE), myelin damage, proinflammatory, an-tigen presenting cells (APCs), macrophages, blood-brain-barrier B, autoimmune, leukocytes, nervous parenchyma, inflammatory mediators, oedema, ischemia, myelin destruction, axonal, T lymphocytes, apoptosis, lymphatic drainage, modus operandi, clinically isolated syndrome (CIS), demyelination, dendritic cells, Acute Disseminated Encephalomyelitis, adenovi-rus, Mycoplasma pneumoniae, Chlamydia pneumoniae, influenza A, influenza B, herpes simplex, encepha-lopathy, hemiparesis, paraparesis, ataxia, systemic lupus erythematosus, Sjögren's syndrome, Acute Idiopathic Inflammatory Polyradiculoneuritis Guil-lain-Barre Syndrome, post-infectious polyneuropathy, arreflexia, acute inflam-matory demyelinating polyradiculoneuropathy, sensory axonal neuropathy, acute motor axonal, acute pan-dysautonomia, Miller Fisher's syndrome, Chronic Inflammatory Demyelinating Polyradiculoneuritis, Corticotherapy, immu-nosuppressant, Intravenous Immunoglobulin, Glatiramer Acetate, Natalizumab


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