ReviewJournal of neurology2026
MOGAD update: new phenotypes in the expanding clinical spectrum.
Review in Journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
2 authors.
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Abstract
Myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD) is often heralded by established clinical features, including optic neuritis (ON), transverse myelitis (TM), cerebral cortical encephalitis, acute disseminated encephalitis (ADEM), and cerebral, brainstem and/or cerebellar defects. Recent publications have revealed new clinical phenotypes that challenge perceptions regarding age of onset, disease progression, and neurologic recovery related to MOGAD relapses. In this review, we use a case-based format to highlight less typical disease manifestations of MOGAD that will likely gain more recognition over time. In so doing, we hope to facilitate earlier diagnosis and more impactful treatment for people with MOGAD (pwMOGAD). Further scientific exploration regarding less common clinical manifestations of MOGAD may inform understanding regarding pathogenicity of the MOG autoantibody, and pathobiological mechanisms that drive disease expression in this intriguing condition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.