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The changing concepts in the neuropathology of acquired demyelinating central nervous system disorders

Lassmann, Hans

Current Opinion in Neurology: June 2019 - Volume 32 - Issue 3 - p 313–319
doi: 10.1097/WCO.0000000000000685
DEMYELINATING DISEASES: Edited by Hans-Peter Hartung
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Purpose of review Research on multiple sclerosis (MS) pathogenesis and therapy is to a large extent driven by results obtained in experimental autoimmune encephalomyelitis (EAE). This approach provided deep insights into the mechanism of brain inflammation and immune mediated tissue injury and, thus, most of our currently established therapies for MS patients have been developed with profound contributions of experimental autoimmune research. Recent data, which are summarized in this review article, however, show important differences between EAE and MS.

Recent findings EAE models perfectly reproduce a disease, now called myelin oligodendrocyte glycoprotein (MOG) antibody-associated inflammatory demyelinating disease, which, however, is different from classical MS. In MS, the inflammatory reaction in the brain is dominated by CD8+ T-lymphocyte and CD20+ B cells. Demyelination in MS appears to be triggered by soluble factors, produced by T cells and/or B cells, which are different from anti-MOG antibodies seen in EAE, and induce widespread MS like primary demyelination and tissue damage associated with oxidative injury, mitochondrial damage and subsequent ‘virtual’ hypoxia.

Summary To define the antigenic target of the inflammatory reaction, the nature of the inflammatory response and the mechanisms of tissue injury are key topics of ongoing MS research.

Center for Brain Research, Medical University of Vienna, Vienna, Austria

Correspondence to Hans Lassmann, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria. Tel: +43 1 40160 34200; e-mail: hans.lassmann@meduniwien.ac.at

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