J. Ko, Ji-Hoon Na, Hyunjoo Lee, J. Byun, Joon Sik Kim, Young-Mock Lee
{"title":"髓鞘少突胶质细胞糖蛋白抗体相关疾病伴急性双侧全盲1例","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":"{\"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}","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}
A Case of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease with Acute Bilateral Total Blindness
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.