MOG antibody disease: A review of MOG antibody seropositive neuromyelitis optica spectrum disorder

•MOG antibody disease is the most recent antigen specific autoimmune disease on the NMO Spectrum.•MOG antibody disease is characterized by optic neuritis and less commonly transverse myelitis with generally better outcomes compared to the AQP4 NMO.•Half of MOG antibody positive cases remain monophas...

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Published inMultiple sclerosis and related disorders Vol. 25; pp. 66 - 72
Main Authors Narayan, Ram, Simpson, Alexandra, Fritsche, Katelyn, Salama, Sara, Pardo, Santiago, Mealy, Maureen, Paul, Friedemann, Levy, Michael
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.10.2018
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Online AccessGet full text
ISSN2211-0348
2211-0356
2211-0356
DOI10.1016/j.msard.2018.07.025

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Abstract •MOG antibody disease is the most recent antigen specific autoimmune disease on the NMO Spectrum.•MOG antibody disease is characterized by optic neuritis and less commonly transverse myelitis with generally better outcomes compared to the AQP4 NMO.•Half of MOG antibody positive cases remain monophasic after the initial attack. MOG antibody disease is an autoimmune disease of the central nervous system associated with a serological antibody against MOG, myelin oligodendrocyte glycoprotein. MOG is a glycoprotein expressed on the outer membrane of myelin and solely found within the central nervous system, including in the brain, optic nerves and spinal cord. Clinically, the disease resembles neuromyelitis optica spectrum disorders in the predilection for relapses of optic neuritis and transverse myelitis. In addition, acute disseminated encephalomyelitis (ADEM) is a well-recognized phenotype of MOG antibody disease in children. In recent studies around the world where MOG testing is available, up to 42% of NMOSD patients who test seronegative for the AQP4 antibody test positive for MOG antibodies. MOG antibody disease has thus recently emerged as a distinct entity carved out of the patient population diagnosed with NMOSD. In this review, we examine the history of the MOG antibody and its relevance to demyelinating disease, as well as compare the clinical, radiographic and serological profiles of patients with MOG antibody with patients with AQP4 antibody.
AbstractList •MOG antibody disease is the most recent antigen specific autoimmune disease on the NMO Spectrum.•MOG antibody disease is characterized by optic neuritis and less commonly transverse myelitis with generally better outcomes compared to the AQP4 NMO.•Half of MOG antibody positive cases remain monophasic after the initial attack. MOG antibody disease is an autoimmune disease of the central nervous system associated with a serological antibody against MOG, myelin oligodendrocyte glycoprotein. MOG is a glycoprotein expressed on the outer membrane of myelin and solely found within the central nervous system, including in the brain, optic nerves and spinal cord. Clinically, the disease resembles neuromyelitis optica spectrum disorders in the predilection for relapses of optic neuritis and transverse myelitis. In addition, acute disseminated encephalomyelitis (ADEM) is a well-recognized phenotype of MOG antibody disease in children. In recent studies around the world where MOG testing is available, up to 42% of NMOSD patients who test seronegative for the AQP4 antibody test positive for MOG antibodies. MOG antibody disease has thus recently emerged as a distinct entity carved out of the patient population diagnosed with NMOSD. In this review, we examine the history of the MOG antibody and its relevance to demyelinating disease, as well as compare the clinical, radiographic and serological profiles of patients with MOG antibody with patients with AQP4 antibody.
Highlights•MOG antibody disease is the most recent antigen specific autoimmune disease on the NMO Spectrum. •MOG antibody disease is characterized by optic neuritis and less commonly transverse myelitis with generally better outcomes compared to the AQP4 NMO. •Half of MOG antibody positive cases remain monophasic after the initial attack.
MOG antibody disease is an autoimmune disease of the central nervous system associated with a serological antibody against MOG, myelin oligodendrocyte glycoprotein. MOG is a glycoprotein expressed on the outer membrane of myelin and solely found within the central nervous system, including in the brain, optic nerves and spinal cord. Clinically, the disease resembles neuromyelitis optica spectrum disorders in the predilection for relapses of optic neuritis and transverse myelitis. In addition, acute disseminated encephalomyelitis (ADEM) is a well-recognized phenotype of MOG antibody disease in children. In recent studies around the world where MOG testing is available, up to 42% of NMOSD patients who test seronegative for the AQP4 antibody test positive for MOG antibodies. MOG antibody disease has thus recently emerged as a distinct entity carved out of the patient population diagnosed with NMOSD. In this review, we examine the history of the MOG antibody and its relevance to demyelinating disease, as well as compare the clinical, radiographic and serological profiles of patients with MOG antibody with patients with AQP4 antibody.MOG antibody disease is an autoimmune disease of the central nervous system associated with a serological antibody against MOG, myelin oligodendrocyte glycoprotein. MOG is a glycoprotein expressed on the outer membrane of myelin and solely found within the central nervous system, including in the brain, optic nerves and spinal cord. Clinically, the disease resembles neuromyelitis optica spectrum disorders in the predilection for relapses of optic neuritis and transverse myelitis. In addition, acute disseminated encephalomyelitis (ADEM) is a well-recognized phenotype of MOG antibody disease in children. In recent studies around the world where MOG testing is available, up to 42% of NMOSD patients who test seronegative for the AQP4 antibody test positive for MOG antibodies. MOG antibody disease has thus recently emerged as a distinct entity carved out of the patient population diagnosed with NMOSD. In this review, we examine the history of the MOG antibody and its relevance to demyelinating disease, as well as compare the clinical, radiographic and serological profiles of patients with MOG antibody with patients with AQP4 antibody.
MOG antibody disease is an autoimmune disease of the central nervous system associated with a serological antibody against MOG, myelin oligodendrocyte glycoprotein. MOG is a glycoprotein expressed on the outer membrane of myelin and solely found within the central nervous system, including in the brain, optic nerves and spinal cord. Clinically, the disease resembles neuromyelitis optica spectrum disorders in the predilection for relapses of optic neuritis and transverse myelitis. In addition, acute disseminated encephalomyelitis (ADEM) is a well-recognized phenotype of MOG antibody disease in children. In recent studies around the world where MOG testing is available, up to 42% of NMOSD patients who test seronegative for the AQP4 antibody test positive for MOG antibodies. MOG antibody disease has thus recently emerged as a distinct entity carved out of the patient population diagnosed with NMOSD. In this review, we examine the history of the MOG antibody and its relevance to demyelinating disease, as well as compare the clinical, radiographic and serological profiles of patients with MOG antibody with patients with AQP4 antibody.
Author Narayan, Ram
Simpson, Alexandra
Pardo, Santiago
Levy, Michael
Fritsche, Katelyn
Paul, Friedemann
Salama, Sara
Mealy, Maureen
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  givenname: Ram
  surname: Narayan
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  organization: Department of Neurology, Johns Hopkins University, Baltimore, MD, USA
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  surname: Simpson
  fullname: Simpson, Alexandra
  organization: Department of Neurology, Johns Hopkins University, Baltimore, MD, USA
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  organization: Department of Neurology, Johns Hopkins University, Baltimore, MD, USA
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  givenname: Sara
  orcidid: 0000-0003-2380-8152
  surname: Salama
  fullname: Salama, Sara
  organization: Department of Neurology, Johns Hopkins University, Baltimore, MD, USA
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  givenname: Santiago
  surname: Pardo
  fullname: Pardo, Santiago
  organization: Department of Neurology, Johns Hopkins University, Baltimore, MD, USA
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  givenname: Maureen
  orcidid: 0000-0001-8967-6338
  surname: Mealy
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  organization: Department of Neurology, Johns Hopkins University, Baltimore, MD, USA
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  givenname: Friedemann
  surname: Paul
  fullname: Paul, Friedemann
  organization: Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, NeuroCure Clinical Research Center, Berlin, Germany
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  givenname: Michael
  orcidid: 0000-0002-7969-8346
  surname: Levy
  fullname: Levy, Michael
  email: mlevy@jhmi.edu
  organization: Department of Neurology, Johns Hopkins University, Baltimore, MD, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30048919$$D View this record in MEDLINE/PubMed
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Popescu (10.1016/j.msard.2018.07.025_bib0057) 2016; 133
Pandit (10.1016/j.msard.2018.07.025_bib0052) 2018; 5
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Mariotto (10.1016/j.msard.2018.07.025_bib0041) 2017; 264
Saini (10.1016/j.msard.2018.07.025_bib0064) 2010; 221
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30384960 - Mult Scler Relat Disord. 2018 Oct;25:A1-A2
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– reference: 30384960 - Mult Scler Relat Disord. 2018 Oct;25:A1-A2
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Snippet •MOG antibody disease is the most recent antigen specific autoimmune disease on the NMO Spectrum.•MOG antibody disease is characterized by optic neuritis and...
Highlights•MOG antibody disease is the most recent antigen specific autoimmune disease on the NMO Spectrum. •MOG antibody disease is characterized by optic...
MOG antibody disease is an autoimmune disease of the central nervous system associated with a serological antibody against MOG, myelin oligodendrocyte...
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SubjectTerms Animals
Autoantibodies - blood
Humans
Myelin-Oligodendrocyte Glycoprotein - immunology
Neurology
Neuromyelitis Optica - blood
Neuromyelitis Optica - immunology
Title MOG antibody disease: A review of MOG antibody seropositive neuromyelitis optica spectrum disorder
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https://dx.doi.org/10.1016/j.msard.2018.07.025
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