Longitudinal Brain Atrophy in Human MS, MOGAD, and AQP4 + NMOSD
In a study of 489 participants, those with Multiple Sclerosis (MS) exhibited faster global brain atrophy compared to controls, while patients with Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) showed white matter volume loss and ventricular enlargement. Individuals with AQP4 + Neuromyelitis Optica Spectrum Disorder (NMOSD) experienced pallidal volume reduction.
- Tags
- #MSResearch
- Most relevant to
- —
- Human efficacy
- Not established from this source
- Mechanism
- Not reported
- Evidence strength
- Not graded
- Outcome
- Not reported
Why it matters
These findings suggest that different demyelinating conditions have distinct patterns of brain atrophy, which could inform understanding of disease progression and might influence future research approaches.
What this does not prove
The study had limitations including a small NMOSD sample size, varied follow-up durations, and potential inconsistencies related to MRI scanner use.
Next milestone
No next milestone was established from the available source.
Study facts
- Study design
- Not reported
- Participants / samples
- 489 · basis not reported
- Randomised
- Not reported
- Controlled
- Not reported
- Primary endpoint met
- Not reported
- Relevant MS type
- Not reported
- Publication date
- 2026-10-20
- Evidence reviewed
- Abstract only
- Regulatory approval
- Not reported
- Research areas
- Not classified
- Biological target
- Not reported
- Pathway
- Not reported
- Population
- Patients with MS, MOGAD, AQP4 + NMOSD; age 18 years or older
- Size of effect
- Not reported
- Secondary endpoints
- Not reported
- MRI endpoints
- Not reported
- Biomarkers
- Not reported
- Safety
- Not reported
Original sources
- Primary evidenceDifferential Trajectories of Brain Atrophy in Multiple Sclerosis, MOGAD, and AQP4 + NMOSD: The Role of Disease Activity in MOGAD. ↗DOI: 10.1212/wnl.0000000000218673
Supporting passages (11)
sample size489
subjectsHuman
speciesHumans
publication date2026-10-20
primary endpointWe aimed to compare longitudinal trajectories of global and regional brain atrophy across MS, MOGAD, and AQP4 + NMOSD and investigate whether atrophy in MOGAD is associated with disease course and lesion dynamics.
follow upThe mean follow-up was MS: 2.44 ± 1.55 years, MOGAD: 2.57 ± 1.85, and AQP4 + NMOSD: 3.22 ± 2.42.
findingsCompared with controls, MS showed accelerated global brain atrophy (β = -2.027 cm3 per year, 95% CI -3.430 to -0.623).
limitationsLimitations include small NMOSD sample, heterogeneous follow-up, and potential scanner-related variability.
populationMETHODS: In this retrospective multicenter Magnetic Resonance Imaging in Multiple Sclerosis (MAGNIMS) study, patients fulfilling the following criteria were enrolled: (1) age 18 years or older, (2) MS/MOGAD/AQP4 + NMOSD diagnosis, (3) ≥2 same-scanner brain MRIs ≥6 months apart and ≥3 months postattack, (4) concurrent Expanded Disability Status Scale, and (5) disease course information.
peer reviewedPublication types: Journal Article; Multicenter Study
subjectsMeSH terms: Humans; Female; Atrophy; Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease; Aquaporin 4; Adult; Brain; Multiple Sclerosis; Male; Magnetic Resonance Imaging; Retrospective Studies; Middle Aged; Neuromyelitis Optica; Disease Progression; Myelin-Oligodendrocyte Glycoprotein
AI assessment, not yet reviewed by a person · version 2 · Community votes are separate from evidence review.