ArticleAnnals of clinical and translational neurology2026
Quantitative MRI Uncovers Subtle Cortical Damage in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.
Article in Annals of clinical and translational 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.
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Abstract
objectiveTo determine whether myelin-sensitive quantitative MRI reveals microstructural abnormalities in normal-appearing cortex (NACtx) in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), indicating that conventional MRI underestimates remission residual cortical injury.
methodsForty-two patients with MOGAD in remission and 42 age- and sex-matched healthy controls (HCs) underwent cognitive testing (Rao Brief Repeatable Battery), disability rating (Expanded Disability Status Scale) and 3-T MRI, including three-dimensional T1-weighted, T2-weighted and double-inversion-recovery sequences to identify cortical lesions and delineate NACtx. T1- to T2-weighted ratio z-scores (T1/T2r), magnetisation transfer ratio (MTR) and magnetisation transfer saturation (MTsat) were derived in global and lobar NACtx; MT imaging was available in 22 patients and 24 controls. Linear mixed-effects models compared MOGAD with HCs and cortical (history of at least one acute cortical attack) with non-cortical phenotypes, adjusting for age, sex, site and cortical thickness with false-discovery-rate correction.
resultsSixteen of 42 MOGAD patients had a cortical phenotype; cortical lesions at remission were present in 4 of 42 (9.5%), all with a cortical phenotype. MTsat metric, but not T1/T2r or MTR, detected NACtx alterations in the MOGAD cohort compared with HCs. Cortical MOGAD phenotype showed reduced MTsat in global, frontal, temporal, limbic, hippocampal and insular NACtx regions vs. HCs, whereas non-cortical MOGAD was similar to HCs. Exploratory analyses suggested lower MTsat in temporal, limbic, hippocampal and insular NACtx regions in cortical MOGAD with cognitive impairment than in cognitively preserved MOGAD.
interpretationMyelin-sensitive MTsat reveals persistent, regionally specific abnormalities in normal-appearing cortex in cortical MOGAD and is a promising marker of residual cortical damage linked to cognitive dysfunction.
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