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Updated: Nov 2, 2025
Human Serum Anti-aquaporin-4 Immunoglobulin G Detection by Cell-based Assay
Published on: April 5, 2019
Comparative study of AQP4-NMOSD, MOGAD and seronegative NMOSD: a single-center Belgian cohort
Solène Dauby1,2, Dominique Dive3, Laurence Lutteri4
1Clinical Neuroimmunology Unit, Department of Neurology, CHU Liège, University Hospital of Liège, Liège, Belgium. solene.dauby@chuliege.be.
Purpose:
To emphasize physio-pathological, clinical and prognosis differences between conditions causing serious and sometimes very similar clinical manifestations: anti-aquaporin-4 (AQP4) and anti-myelin oligodendrocyte glycoprotein (MOG) antibodies related diseases, and seronegative NMOSD (neuromyelitis optica spectrum disorders).
Methods:
Based on Wingerchuk et al. (Neurology 85:177-189, 2015) criteria for NMOSD and on those more recently proposed by Jarius et al. (J Neuroinflammation 15:134, 2018) for MOGAD (MOG associated disorders), we retrospectively surveyed 10 AQP4-NMOSD, 8 MOGAD and 2 seronegative NMOSD, followed at the specialized neuroimmunology unit of the CHU Liège.
Results:
Female predominance was only observed in AQP4 group. Age at onset was 37.8 and 27.7 years old for AQP4-NMOSD and MOGAD respectively. In both groups, the first clinical event most often consisted of optic neuritis (ON), followed by isolated myelitis. Fifteen of our 20 patients encountered a relapsing course with 90% relapses in AQP4-NMOSD, 62.5% in MOGAD and 50% in seronegative group, and a mean period between first and second clinical event of 7.1 and 4.8 months for AQP4-NMOSD and MOGAD, respectively. In total we counted 54 ON, with more ON per patient in MOGAD. MOG-associated ON mainly affected the anterior part of the optic nerve with a papilledema in 79.2% of cases. Despite a fairly good visual outcome after MOG-associated ON, retinal nerve fibre layer (RNFL) thickness decreased, suggesting a fragility of the optic nerve toward further attacks.
Conclusion:
As observed in larger cohorts, our MOGAD and AQP4-NMOSD cases differ by clinical and prognostic features. A better understanding of these diseases should encourage prompt biological screening and hasten proper diagnosis and treatment.
Insights
This study differentiates anti-aquaporin-4 (AQP4) and anti-myelin oligodendrocyte glycoprotein (MOG) antibody diseases from seronegative neuromyelitis optica spectrum disorders (NMOSD). Understanding these differences aids in prompt diagnosis and treatment for better patient outcomes.
Area of Science:
- Neuroimmunology
- Neurology
- Clinical Medicine
Background:
- Neuromyelitis optica spectrum disorders (NMOSD) encompass conditions with similar clinical presentations but distinct underlying pathologies.
- Differentiating between anti-aquaporin-4 (AQP4) antibody disease, anti-myelin oligodendrocyte glycoprotein (MOG) antibody disease (MOGAD), and seronegative NMOSD is crucial for accurate diagnosis and management.
Purpose of the Study:
- To highlight the key physio-pathological, clinical, and prognostic distinctions between AQP4-NMOSD, MOGAD, and seronegative NMOSD.
- To emphasize the importance of accurate diagnostic classification for these severe neurological conditions.
Main Methods:
- Retrospective analysis of 10 AQP4-NMOSD, 8 MOGAD, and 2 seronegative NMOSD patients.
- Utilized Wingerchuk et al. (2015) criteria for NMOSD and Jarius et al. (2018) criteria for MOGAD.
Main Results:
- Female predominance was noted in the AQP4 group. Mean age at onset was 37.8 years for AQP4-NMOSD and 27.7 years for MOGAD.
- Optic neuritis (ON) and isolated myelitis were common initial events. Relapsing courses were observed in 90% of AQP4-NMOSD, 62.5% of MOGAD, and 50% of seronegative NMOSD patients.
- MOGAD-associated ON frequently affected the anterior optic nerve with papilledema, leading to RNFL thinning despite good initial visual recovery, indicating optic nerve vulnerability.
Conclusions:
- Clinical and prognostic features differentiate MOGAD and AQP4-NMOSD, consistent with larger cohort findings.
- Enhanced understanding of these distinct disease entities necessitates prompt biological screening for accurate diagnosis and timely treatment initiation.
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