We are analyzing https://link.springer.com/article/10.1007/s00415-023-11737-8.

Title:
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): current understanding and challenges | Journal of Neurology
Description:
New diagnostic criteria for myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) have recently been proposed, distinguishing this syndrome from other inflammatory diseases of the central nervous system. Seropositivity status for MOG-IgG autoantibodies is important for diagnosing MOGAD, but only in the context of robust clinical characterization and cautious interpretation of neuroimaging. Over the last several years, access to cell-based assay (CBA) techniques has improved diagnostic accuracy, yet the positive predictive value of serum MOG-IgG values varies with the prevalence of MOGAD in any given patient population. For this reason, possible alternative diagnoses need to be considered, and low MOG-IgG titers need to be carefully weighted. In this review, cardinal clinical features of MOGAD are discussed. Key challenges to the current understanding of MOGAD are also highlighted, including uncertainty regarding the specificity and pathogenicity of MOG autoantibodies, the need to identify immunopathologic targets for future therapies, the quest to validate biomarkers that facilitate diagnosis and detect disease activity, and the importance of deciphering which patients with MOGAD require long-term immunotherapy.
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Keywords {🔍}

article, pubmed, google, scholar, neurol, myelin, oligodendrocyte, glycoprotein, cas, disease, central, optic, mogad, disorders, neuritis, antibodyassociated, treatment, chen, clinical, httpsdoiorgs, neuromyelitis, optica, mogigg, mog, patients, spectrum, neurology, disorder, costello, jama, review, antibody, neuroinflammation, diseases, study, international, httpsdoiorgwnl, acute, mogiggassociated, diagnostic, criteria, inflammatory, access, diagnosis, longterm, antibodies, ophthalmol, mult, scler, neurosurg,

Topics {✒️}

month download article/chapter central nervous system idiopathic inflammatory-demyelinating diseases myelin-oligodendrocyte glycoprotein antibody myelin oligodendrocyte glycoprotein-immunoglobulin myelin oligodendrocyte glycoprotein-igg myelin oligodendrocyte glycoprotein-igg steroid-sparing maintenance immunotherapy clinically defined mog-ad neuro-ophthalmology publish ah low mog-igg titers persistent mog-igg positivity inflammatory demyelinating diseases abdullah al-ani central vein sign myelin oligodendrocyte glycoprotein myelin oligodendrocyte glycoprotein article al-ani meta-analysis neuro-inflammation full article pdf disorder versus aquaporin-4-igg treatment-refractory mog-igg 1186/s12974-016-0718-0 stiebel-kalish optical coherence tomography personal data related subjects privacy choices/manage cookies ethics statement real-world cohort tobin wo cobo calvo á apóstolos-pereira sl relapsing mog antibody data protection long-term immunotherapy 1136/jnnp-2022-330237 lopez-chiriboga aquaporin-4 antibody diseases accepted manuscript version mog antibody assays mog-antibody titres neurological update access relapsing mog-igg cns inflammatory diseases mri lesion evolution opsoclonus–myoclonus syndrome standardized mri protocol neurofilament light chain neuro-oncologic emergency mog antibody disease mog-antibody disease

Questions {❓}

Abrams RMC, Safavi F, Tuhrim S et al (2021) MRI negative myelopathy post mild SARS-CoV-2 infection: vasculopathy or inflammatory myelitis?
Havla J, Pakeerathan T, Schwake C et al (2021) Age-dependent favorable visual recovery despite significant retinal atrophy in pediatric MOGAD: how much retina do you really need to see well?
Kunchok A, Krecke KN, Flanagan EP et al (2020) Does area postrema syndrome occur in myelin oligodendrocyte glycoprotein-IgG–associated disorders (MOGAD)?
Stiebel-Kalish H, Hellmann MA, Mimouni M, et al (2019) Does time equal vision in the acute treatment of a cohort of AQP4 and MOG optic neuritis?

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         description:New diagnostic criteria for myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) have recently been proposed, distinguishing this syndrome from other inflammatory diseases of the central nervous system. Seropositivity status for MOG-IgG autoantibodies is important for diagnosing MOGAD, but only in the context of robust clinical characterization and cautious interpretation of neuroimaging. Over the last several years, access to cell-based assay (CBA) techniques has improved diagnostic accuracy, yet the positive predictive value of serum MOG-IgG values varies with the prevalence of MOGAD in any given patient population. For this reason, possible alternative diagnoses need to be considered, and low MOG-IgG titers need to be carefully weighted. In this review, cardinal clinical features of MOGAD are discussed. Key challenges to the current understanding of MOGAD are also highlighted, including uncertainty regarding the specificity and pathogenicity of MOG autoantibodies, the need to identify immunopathologic targets for future therapies, the quest to validate biomarkers that facilitate diagnosis and detect disease activity, and the importance of deciphering which patients with MOGAD require long-term immunotherapy.
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      headline:Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): current understanding and challenges
      description:New diagnostic criteria for myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) have recently been proposed, distinguishing this syndrome from other inflammatory diseases of the central nervous system. Seropositivity status for MOG-IgG autoantibodies is important for diagnosing MOGAD, but only in the context of robust clinical characterization and cautious interpretation of neuroimaging. Over the last several years, access to cell-based assay (CBA) techniques has improved diagnostic accuracy, yet the positive predictive value of serum MOG-IgG values varies with the prevalence of MOGAD in any given patient population. For this reason, possible alternative diagnoses need to be considered, and low MOG-IgG titers need to be carefully weighted. In this review, cardinal clinical features of MOGAD are discussed. Key challenges to the current understanding of MOGAD are also highlighted, including uncertainty regarding the specificity and pathogenicity of MOG autoantibodies, the need to identify immunopathologic targets for future therapies, the quest to validate biomarkers that facilitate diagnosis and detect disease activity, and the importance of deciphering which patients with MOGAD require long-term immunotherapy.
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