ArticleAnnals of clinical and translational neurology2025
Understanding Mechanisms of Whole Brain and Regional Grey Matter Atrophy in Children With MOGAD.
Article in Annals of clinical and translational neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Targeting Lifestyle in CNS Inflammatory Demyelinating Diseases: Insights from Diet and Exercise as Potential Disease Modifiers.Brain sciences · 2025Review
- Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Pathophysiology, Clinical Patterns, and Therapeutic Challenges of Intractable and Severe Forms.International journal of molecular sciences · 2025Review
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15 authors.
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Abstract
objectiveTo investigate the mechanisms driving whole brain and regional grey matter (GM) volume changes along with their clinical correlates in paediatric myelin oligodendrocyte glycoprotein antibody (MOG-Ab)-associated disease (MOGAD).
methodsOne-hundred-nine paediatric MOGAD patients from two UK centres underwent MRI at attack nadir and follow-up (at least 1) ≥ 6 weeks later. Normative trajectories from 317 typically developing children informed volumetric comparisons. MRI segmentation with SynthSeg+ enabled volumetric analysis. Linear mixed-effects models examined impact of brain lesions, disease course, MOG-Ab serostatus and age at onset on brain volumes and changes over time, along with clinical correlates.
resultsBrain lesions were present in 71/109 patients, who were younger and more likely to present with acute disseminated encephalomyelitis. At onset, 79% showed reduced brain growth, particularly those with brain lesions. Over time, 46% developed atrophy, associated with lesion presence and relapsing disease. All patients exhibited cortical and deep GM growth reduction at onset, with brain lesions driving progressive atrophy. Brian lesion complete resolution mitigated atrophy in the left supramarginal and right inferior parietal gyri. Relapsing disease was linked to greater GM atrophy in the frontal, temporal and parietal lobes. Persistent MOG-Ab positivity correlated with GM atrophy in the cingulate and entorhinal cortices and temporal pole. Disability progression was linked to deep GM, temporal pole and lateral orbitofrontal atrophy, while learning difficulties were associated with lateral occipital and parietal atrophy.
interpretationBrain lesions at onset and their persistence, relapsing disease and MOG-Ab positivity are key risk factors for GM atrophy and clinical impairment in paediatric MOGAD.
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