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The Role of Iron in the Pathogenesis of Experimental Allergic Encephalomyelitis and Multiple Sclerosis
Author(s) -
LEVINE STEVEN M.,
CHAKRABARTY ANURADHA
Publication year - 2004
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1306.021
Subject(s) - pathogenesis , multiple sclerosis , myelin , encephalomyelitis , experimental autoimmune encephalomyelitis , ferritin , immunology , microglia , gliosis , central nervous system , transferrin , chemistry , medicine , neuroscience , biology , pathology , biochemistry , inflammation
A bstract : Multiple sclerosis (MS) and its animal model, experimental allergic encephalomyelitis (EAE), are autoimmune disorders resulting in demyelination in the central nervous system (CNS). Pathologically, the blood‐brain barrier becomes damaged, macrophages and T cells enter into the CNS, oligodendrocytes and myelin are destroyed, astrocytes and microglia undergo gliosis, and axons become transected. Data from several biochemical and pharmacological studies indicate that free radicals participate in the pathogenesis of EAE, and iron has been implicated as the catalyst leading to their formation. The primary focus of this article is the examination of the role of iron in the pathogenesis of MS and EAE. Particular attention will be paid to the role and distribution of iron and proteins involved with iron metabolism (e.g., transferrin, ferritin, heme oxygenase‐1, etc.) in normal and disease states of myelin. Furthermore, therapeutic interventions aimed at iron, iron‐binding proteins, and substrates or products of iron‐catalyzed reactions leading to free radical production will be discussed.