J. Ko, Ji-Hoon Na, Hyunjoo Lee, J. Byun, Joon Sik Kim, Young-Mock Lee
{"title":"A Case of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease with Acute Bilateral Total Blindness","authors":"J. Ko, Ji-Hoon Na, Hyunjoo Lee, J. Byun, Joon Sik Kim, Young-Mock Lee","doi":"10.26815/acn.2022.00143","DOIUrl":null,"url":null,"abstract":"Myelin oligodendrocyte glycoprotein (MOG) an-tibody-associated disease (MOGAD) is a demyelinating disease of the central nervous system. MOG is a glycoprotein located on the surface of oligodendrocytes that acts as a cellular adhesive molecule in the central nervous system. The role of MOG has not been fully elucidated, but it is known to regulate microtubule stability and mod-ulate myelin-immune interactions by mediating the complement cascade [1]. MOGAD clinically presents with optic neuritis, transverse myelitis (TM), or rarely, acute disseminated encephalomy-elitis (ADEM), depending on the location of the lesion. The clinical manifestations of MOGAD differ by age. Younger children mostly present with an ADEM phenotype.","PeriodicalId":33305,"journal":{"name":"Annals of Child Neurology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of Child Neurology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.26815/acn.2022.00143","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 1
Abstract
Myelin oligodendrocyte glycoprotein (MOG) an-tibody-associated disease (MOGAD) is a demyelinating disease of the central nervous system. MOG is a glycoprotein located on the surface of oligodendrocytes that acts as a cellular adhesive molecule in the central nervous system. The role of MOG has not been fully elucidated, but it is known to regulate microtubule stability and mod-ulate myelin-immune interactions by mediating the complement cascade [1]. MOGAD clinically presents with optic neuritis, transverse myelitis (TM), or rarely, acute disseminated encephalomy-elitis (ADEM), depending on the location of the lesion. The clinical manifestations of MOGAD differ by age. Younger children mostly present with an ADEM phenotype.