[Pathogenesis of neuromyelitis optica].

Tatsuro Misu, Kazuo Fujihara

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

Neuromyelitis optica (NMO) is a disease characterized by severe optic neuritis and transverse myelitis with autoantibody against aquaporin 4 (AQP4), mainly localized at astrocyte foot processes. Loss of AQP4 and glial fibrillary acidic protein with relatively preserved myelin is the pathological hallmarks of active NMO lesions. Several experimental studies suggested the crucial role of AQP4 antibody with diverse mechanisms including antibody- and complement-induced cytotoxicity against astrocytes. In vivo studies demonstrated that T cell-mediated CNS inflammation is necessary for the access of AQP4 antibody into CNS. NMO patients often develop medullary lesions including area postrema, which lacks the blood-brain-barrier and is sensitive to emetic agents. NMO is now considered to be an autoimmune astrocytopathy, and is distinct from multiple sclerosis.

Original languageEnglish
Pages (from-to)823-828
Number of pages6
JournalUnknown Journal
Volume71
Issue number5
Publication statusPublished - 2013 May

ASJC Scopus subject areas

  • Medicine(all)

Fingerprint Dive into the research topics of '[Pathogenesis of neuromyelitis optica].'. Together they form a unique fingerprint.

  • Cite this

    Misu, T., & Fujihara, K. (2013). [Pathogenesis of neuromyelitis optica]. Unknown Journal, 71(5), 823-828.