Abstract
Background
Large-scale studies examining the demographic, serological, and seasonal characteristics of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and aquaporin-4 immunoglobulin G-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD) remain limited, despite their potential to provide crucial information for resource allocation, clinical trial design, and recruitment.
Objective
To investigate demographic, serological, and seasonal variations in MOGAD and AQP4+NMOSD using a large neuroimmunology laboratory registry validated by clinical cohorts.
Methods
We conducted a retrospective, laboratory-based study using data from the Mayo Clinic Neuroimmunology Laboratory registry and clinical cohorts between July 2014 and April 2024. The first available serum sample from each patient tested for MOG-IgG and AQP4-IgG was included. Analyses focused on age and sex distributions, antibody titers, and seasonal patterns of seropositivity, as well as the month and season of disease onset and attacks among the clinical cohorts of MOGAD and AQP4+NMOSD.
Results
We included 89,495 sera tested for MOG-IgG and 198,401 for AQP4-IgG, supplemented by validated clinical cohorts of 528 patients with MOGAD and 534 with AQP4+NMOSD. MOG-IgG was detected in 6,313 samples (7.1%), with 1,566 (24.8%) exhibiting high titers (≥1:1,000). AQP4-IgG was positive in 5,057 samples (2.5%). Individuals with MOG-IgG positivity were younger than those with AQP4-IgG positivity (mean age, 34.1 years [SD=20.0] vs 47.7 years [SD=17.9]; p<0.0001). The frequency of MOG-IgG positivity was highest among patients younger than 12 years (1,052 [17.9%]) and declined with older age, while AQP4-IgG positivity increased with older age. AQP4-IgG revealed a strong female predilection (female-to-male ratio 6.2:1), varying by age, whereas MOG-IgG showed a modest female predominance (female-to-male ratio 1.5:1), consistent across all ages. MOG-IgG-titers peaked in younger children and older adults, while AQP4-IgG titers remained stable across ages. Both diseases showed a winter peak in seropositivity, disease onset, and relapses.
Conclusions
This large-scale registry analysis provides comprehensive demographic and serological characterization of MOGAD and AQP4+NMOSD. The modest winter peak suggests that seasonal infectious triggers may play an important role in disease pathogenesis. Limitations include incomplete clinical information within the laboratory registry and a referral-based testing population. These findings have important implications for healthcare planning and optimization of clinical trial design and recruitment.
Keywords: myelin oligodendrocyte glycoprotein, MOG, myelin oligodendrocyte glycoprotein antibody-associated disease, MOGAD, aquaporin-4, AQP4, neuromyelitis optica spectrum disorder, NMOSD, serology, seasonality
Search Terms: [42] Devic’s syndrome, [40] All Demyelinating disease (CNS), [132] Autoimmune diseases, [131] All Immunology
Introduction
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and aquaporin-4-IgG-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD) are autoimmune demyelinating diseases,1,2 for which data on age distribution, sex ratios, titers, and seasonality are variable.3–10 Large-scale analyses could yield more precise estimates. Herein, we used a large laboratory registry to evaluate age, sex, titers, and seasonality in MOGAD and AQP4+NMOSD, validating with clinical cohorts.
Methods
This retrospective study analyzed data from the Mayo Clinic Neuroimmunology Laboratory registry and clinical cohorts (July 2014-April 2024) (eFigure 1). Seasons were defined as winter (December-February), spring (March-May), summer (June-August), and fall (September-November).
Laboratory registry
The Mayo Clinic Neuroimmunology Laboratory’s geographic distribution of samples is outlined in eTable 1. We examined 89,495 MOG-IgG and 198,401 AQP4-IgG tests performed using flow cytometry live cell-based-assays (CBAs), with positivity cutoffs of ≥1:20 and ≥1:5, respectively.11,12 Only the first positive sample per patient was included. Age, sex, antibody titers, dates of collection, and submitting locations were collected.
Clinical cohorts
We validated our laboratory registry findings using clinical cohorts of MOGAD (n=528) and AQP4+NMOSD (n=534) seen at Mayo Clinic or enrolled in our research program from external USA institutions. Clinical data were retrospectively extracted from electronic medical records, and age, sex, antibody titers, disease onset, and attack timing were collected. Attacks were defined by final assessment of the patient’s provider.
Statistical analysis
Data was summarized using means, standard deviations (SDs), frequencies, percentages, and female-to-male ratios. We compared the odds of MOG-IgG and AQP4-IgG positivity by age, sex, and season using logistic regression models, reporting odds ratios (ORs) along with 95% confidence intervals (CIs). Subgroup analyses included assessment of clearly positive MOG-IgG titers (≥1:100) per MOGAD diagnostic criteria1 and MOG-IgG titers ≥1:1,000.11 Age, sex, and seasonal distribution (for Northern Hemisphere only) were compared between groups using two-sample t-tests or chi-square tests, as appropriate. Considering all attacks, season was compared between the clinical cohorts using logistic regression with generalized estimating equations (GEE) to account for within-patient correlation. All statistical testing was two-sided, with significance level of p≤0.05, using SAS 9.4, BlueSky 10.3.1, and R 4.4.1.
Standard Protocol Approvals, Registrations, and Patient Consents
The study was approved by the Mayo Clinic Institutional Review Board. All patients in the clinical cohorts consented to passive use of their clinical records for research purposes. Demographic and antibody titer data from the Neuroimmunology Laboratory registry were collected under a waiver of consent.
Data availability
Anonymized study data are available upon reasonable request from the corresponding authors.
Results
Details of the population tested in the laboratory registry (Table 1)
Table 1:
Demographics of patients tested for MOG-IgG and AQP4-IgG in the laboratory registry
| MOG-IgG | AQP4-IgG | |||||
|---|---|---|---|---|---|---|
| All Tests1 (N=89,495) |
Positive Results1 (N=6,313, 7.1%) |
All Tests1 (N=198,401) |
Positive Results1 (N=5,057, 2.5%) |
|||
| Age, mean (SD) | 41.0 (18.9) | 34.1 (20.0) | 42.4 (17.8) | 47.7 (17.9) | ||
| Age distribution of tested subjects, N (%) | ||||||
| <12 | 5,887 (6.6) | 1,052 (16.7) | 8,415 (4.2) | 98 (1.9) | ||
| 12–17 | 6,423 (7.2) | 663 (10.5) | 10,366 (5.2) | 151 (3.0) | ||
| 18–34 | 20,785 (23.2) | 1,573 (24.9) | 48,237 (24.3) | 1,040 (20.6) | ||
| 35–49 | 25,596 (28.6) | 1,416 (22.4) | 60,632 (30.6) | 1,291 (25.6) | ||
| 50–64 | 20,169 (22.5) | 1,145 (18.1) | 47,344 (23.9) | 1,489 (29.5) | ||
| ≥65 | 10,620 (11.9) | 464 (7.3) | 23,364 (11.8) | 977 (19.4) | ||
| Sex, N (%) | ||||||
| Female | 57,762 (64.9) | 3,757 (59.7) | 130,770 (66.1) | 4,319 (86.1) | ||
| Male | 31,286 (35.1) | 2,537 (40.3) | 67,029 (33.9) | 695 (13.9) | ||
| F:M ratio | 1.9:1 | 1.5:1 | 2.0:1 | 6.2:1 | ||
| Season, N (%)2 | ||||||
| Summer | 22,895 (25.6) | 1,500 (23.8) | 52,637 (26.7) | 1,208 (24.5) | ||
| Fall | 20,878 (23.3) | 1,498 (23.7) | 48,783 (24.8) | 1,263 (25.6) | ||
| Winter | 23,808 (26.6) | 1,762 (27.9) | 51,481 (26.1) | 1,392 (28.2) | ||
| Spring | 21,912 (24.5) | 1,553 (24.6) | 44,148 (22.4) | 1,071 (21.7) | ||
| Titer ≥1:1,000, N (%)3 | NA | 1,566 (24.8) | NA | 3,656 (72.3) | ||
| Screening Result Comparisons | Summary of MOG-IgG | OR (95% CI)4 |
P-value | Summary of AQP4-IgG | OR (95% CI)4 |
P-value |
| Sex, N (% positivity) | ||||||
| Male | 2,537 (8.1) | Reference | 695 (1.0) | Reference | ||
| Female | 3,757 (6.5) | 0.79 (0.75, 0.83) | <0.0001 | 4,319 (3.3) | 3.26 (3.01, 3.53) | <0.0001 |
| Age category, N (% positivity) | ||||||
| <12 | 1,052 (17.9) | Reference | 98 (1.2) | Reference | ||
| 12–17 | 663 (10.3) | 0.53 (0.48, 0.59) | <0.0001 | 151 (1.5) | 1.25 (0.97, 1.62) | 0.08 |
| 18–34 | 1,573 (7.6) | 0.38 (0.35, 0.41) | <0.0001 | 1,040 (2.2) | 1.87 (1.52, 2.30) | <0.0001 |
| 35–49 | 1,416 (5.5) | 0.27 (0.25, 0.29) | <0.0001 | 1,291 (2.1) | 1.85 (1.50, 2.27) | <0.0001 |
| 50–64 | 1,145 (5.7) | 0.28 (0.25, 0.30) | <0.0001 | 1,489 (3.1) | 2.76 (2.24, 3.38) | <0.0001 |
| ≥65 | 464 (4.4) | 0.21 (0.19, 0.24) | <0.0001 | 977 (4.2) | 3.70 (3.00, 4.56) | <0.0001 |
| Season, N (% positivity)2 | ||||||
| Summer | 1,500 (6.6) | Reference | 1,208 (2.3) | Reference | ||
| Fall | 1,498 (7.2) | 1.10 (1.02, 1.19) | 0.01 | 1,263 (2.6) | 1.13 (1.05, 1.23) | 0.002 |
| Winter | 1,762 (7.4) | 1.14 (1.06, 1.22) | 0.0003 | 1,392 (2.7) | 1.18 (1.09, 1.28) | <0.0001 |
| Spring | 1,553 (7.1) | 1.09 (1.01, 1.17) | 0.02 | 1,071 (2.4) | 1.06 (0.97, 1.15) | 0.18 |
Abbreviations: MOG; myelin oligodendrocyte glycoprotein, AQP4; aquaporin-4, F:M ratio; female-to-male ratio, SD; standard deviations, CI; confidence interval, NA; not applicable.
Age and/or sex were not known for all specimens (summarized only when known)
Season analyzed among those tested in the Northern Hemisphere.
Titers summarized among those with a positive screening result.
Odds ratios and corresponding 95% confidence interval (CI) from logistic regression models comparing the odds of positivity.
Among 89,495 sera tested for MOG-IgG, 6,313 (7.1%) were positive, and 1,566 (24.8%) exhibited high titers (≥1:1,000). The mean age at testing was 41.0 years (SD=18.9), with slightly more females tested (female-to-male ratio 1.9:1). Among 198,401 sera tested for AQP4-IgG, 5,057 (2.5%) were positive. The mean age at testing was 42.4 years (SD=17.8), with slightly more females tested (female-to-male ratio 2:1).
MOG-IgG positivity predominates in younger ages; AQP4-IgG in older ages
In the laboratory registry, the mean age of MOG-IgG-positive individuals (34.1 years [SD=20.0]) was lower than that of MOG-IgG-negative individuals (41.6 years [SD=18.7]; p<0.0001) and AQP4-IgG-positive individuals (47.7 years [SD=17.9]; p<0.0001). MOG-IgG positivity was highest among young children (<12 years; 1,052 [17.9%]) and declined with age (≥65 years; 464 [4.4%]; p<0.0001), while AQP4-IgG positivity increased with age (<12 years; 98 [1.2%] versus ≥65 years; 977 [4.2%]; p<0.0001; Table 1, Figure 1A). In the clinical cohorts, MOGAD was more broadly distributed across ages, whereas AQP4+NMOSD was overrepresented in adults (eTable 2, Figure 1B).
Figure 1: Demographics of patients tested for MOG-IgG and AQP4-IgG in the laboratory registry and MOGAD and AQP4+NMOSD patients in the clinical cohorts.
A: Rate of MOG-IgG and AQP4-IgG positivity by age in the laboratory registry,
B: Age distribution of MOGAD and AQP4+NMOSD patients in the clinical cohorts,
C: Sex distribution of MOG-IgG and AQP4-IgG positivity in the laboratory registry,
D: Sex distribution of MOGAD and AQP4+NMOSD patients in the clinical cohorts.
Abbreviations: MOG; myelin oligodendrocyte glycoprotein, AQP4; aquaporin-4, MOGAD; myelin oligodendrocyte glycoprotein antibody-associated disease, AQP4+NMOSD; aquaporin-4 immunoglobulin G-positive neuromyelitis optica spectrum disorder.
AQP4-IgG positivity shows a stronger female predominance
In the laboratory registry, AQP4-IgG-positive cases exhibited a strong female predilection (female-to-male ratio 6.2:1), especially in the 18–64-year age group. MOG-IgG positivity showed a modest female predominance (female-to-male ratio 1.5:1), which persisted in the high-titer subgroup (≥1:1,000; Table 1, Figure 1C). Female-to-male ratios in the clinical cohorts were consistent with the laboratory registry (eTable 2, Figure 1D).
High MOG-IgG titers are more frequent in pediatric patients
In the laboratory registry, MOG-IgG titers (≥1:1,000) were more common in young children (Figure 1A, eFigure 2A) but predominated among older adults in the clinical cohort (eFigure 2B). AQP4-IgG titers were evenly distributed across age groups in both datasets (eFigures 2C–D).
MOG-IgG and AQP4-IgG positivity show a seasonal peak during winter
In the laboratory registry, MOG-IgG and AQP4-IgG positivity were modestly more frequent during winter (versus summer; OR 1.14 and 1.18, respectively; p<0.001), peaking in January and December (Table 1, Figures 2A–B). Clinical cohorts of MOGAD and AQP4+NMOSD also showed a similarly higher frequency of disease onset (124 [28.8%] and 105 [31.4%], respectively) and subsequent attacks (302 [28.4%] and 403 [26.2%], respectively) during winter (eTable 2, Figures 2C–D, eFigures 3A–B).
Figure 2: Seasonal distribution of MOG-IgG and AQP4-IgG positivity in the laboratory registry and onset of MOGAD and AQP4+NMOSD patients in the clinical cohorts.
A: Seasonal distribution of MOG-IgG and AQP4-IgG positivity in the laboratory registry,
B: Monthly distribution of MOG-IgG and AQP4-IgG positivity in the laboratory registry,
C: Seasonal distribution of onset in MOGAD and AQP4+NMOSD patients in the clinical cohorts,
D: Monthly distribution of onset in MOGAD and AQP4+NMOSD patients in the clinical cohorts.
Abbreviations: MOG; myelin oligodendrocyte glycoprotein, AQP4; aquaporin-4, MOGAD; myelin oligodendrocyte glycoprotein antibody-associated disease, AQP4+NMOSD; aquaporin-4 immunoglobulin G-positive neuromyelitis optica spectrum disorder.
Discussion
This study of approximately 300,000 sera tested for MOG-IgG and AQP4-IgG, with 11,000 seropositives validated with 1,000 clinically defined MOGAD and AQP4+NMOSD patients, had four major findings. First, MOG-IgG positivity was most common in children, whereas AQP4-IgG positivity predominated in middle-aged adults. Second, AQP4-IgG positivity showed marked female predominance, while MOG-IgG had a modest female predilection. Third, MOG-IgG titers were highest among younger children and older adults. Finally, we observed a modest winter peak in positivity rates, disease onset, and relapses in both MOGAD and AQP4+NMOSD.
Children accounted for approximately 27% of MOG-IgG-positives versus 5% of AQP4-IgG-positives, underscoring MOGAD’s pediatric predilection, though adults predominated overall (MOGAD≈75%; AQP4+NMOSD 90–95%). The 17.9% MOG-IgG positivity rate in children <12 years approximates the previously reported 25.5% in those <10 years,3 underscoring the importance of including children in future MOGAD clinical trials. The observed mean ages for MOGAD (34–36 years) and AQP4+NMOSD (42–48 years) aligned with prior reports.4,6
The female-to-male ratio of 6.2:1 in AQP4+NMOSD offers a more precise estimate than earlier studies, which ranged from 5:1–9:1.6,13,e1 This strong female predominance, particularly from age 12–64 years, may suggest a role for sex hormones in pathogenesis, as previously postulated.14 Notably, the slight female predominance in MOGAD helps clarify previously conflicting findings.5,6
Our study identified higher MOG-IgG titers among both young children and older adults, whereas prior studies found no differences.15 We speculate the immature immune system or heightened infection risk in young children could predispose, while immunosenescence and immune dysregulation may explain the predilection in older adults.
MOG-IgG positivity rates, disease onset, and relapses peaked in winter, albeit modestly, aligning with studies from Japan and Italy7,9 but differing from the UK;8 similar findings were observed for AQP4-IgG, consistent with prior literature.8,10 We hypothesize that viruses, more frequent during colder seasons, may trigger MOGAD or AQP4+NMOSD attacks, with regional variations in infection types contributing to differing epidemiological patterns and similar seasonality occurs in anti-NMDA-receptor encephalitis.e2 Seasonal differences were overall modest, and attacks occurred in all months and differences were small. Of clinical relevance, preemptive vaccination against seasonal infections and investigating infectious triggers during winter attacks may be valuable, while distinguishing these from pseudorelapses triggered by infections is essential. Reduced vitamin D from decrease sun exposure in winter is an alternative hypothesis reported in multiple sclerosis.e3
This study has limitations. The absence of clinical details in the laboratory registry could have led to the inclusion of false positives; however, high MOG-IgG titers (≥1:1,000) were consistent with overall registry findings, and false positives at this cutoff for MOG-IgG or for AQP4-IgG CBA (any titer) are extremely rare (<0.1%).11,12 The laboratory registry lacked precise information on attack timing but aligned with the clinical cohorts. Referral bias may have impacted the clinical cohort.
In summary, this study provides valuable demographic, seasonal, and serological insights that enable healthcare planning and inform design and recruitment of future clinical trials.
Supplementary Material
Acknowledgment:
This research was supported by Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology in Rochester, MN, USA.
Study Funding:
This study was funded by a research grant from Roche and supported by an NIH grant R01NS113828.
Disclosure:
Nisa Vorasoot reports no disclosures relevant to the manuscript; Matthew C. Edmond reports no disclosures relevant to the manuscript; Sarah M. Jenkins reports no disclosures relevant to the manuscript; Laura Cacciaguerra reports no disclosures relevant to the manuscript; Masoud Majed reports no disclosures relevant to the manuscript; Amy C. Kunchok has received compensation for scientific advisory board for Alexion and for serving as Editor of Neurology: Open Access; John J. Chen reports payment for consultation from UCB, Horizon, and Roche; Jan-Mendelt Tillema is Associate Editor for Journal of Child Neurology; Natthapon Rattanathamsakul reports no disclosures relevant to the manuscript; James P. Fryer has received intellectual property interests from a discovery or technology relating to health care; John R. Mills reports grant support from Werfen Diagnostics. He has patents issued related to the measurement of immunoglobulins by mass spectrometry for which he receives royalties. He also has patents pending for LUZP4-IgG, Cavin-4-IgG, and SKOR2-IgG as markers of neurological autoimmunity; Sarosh R. Irani has received honoraria/research support from UCB, Immunovant, MedImmun, Roche, Janssen, Cerebral therapeutics, ADC therapeutics, Brain, CSL Behring, and ONO Pharma, and receives licensed royalties on patent application WO/2010/046716 entitled ‘Neurological Autoimmune Disorders’ and has filed two other patents entitled “Diagnostic method and therapy” (WO2019211633 and US-2021-0071249-A1; PCT application WO202189788A1) and “Biomarkers” (PCT/GB2022/050614 and WO202189788A1); Sean J. Pittock reports grants, personal fees, and non-financial support from Alexion Pharmaceuticals; grants, personal fees, and non-financial support from MedImmune /Viela Bio; grants, personal fees, and non-financial support from Genentech, Roche; grants from Adimune, and personal fees for consulting from UCB, Astellas and Arialys and Sage Therapeutics. He has two patents issued (8889102; application 12-678350; Neuromyelitis Optica Autoantibodies as a Marker for Neoplasia; and 9891219B2; application 12-573942; Methods for Treating Neuromyelitis Optica [NMO] by Administration of Eculizumab to an individual that is Aquaporin-4 [AQP4]-IgG Autoantibody positive) for which he has received royalties. SJP also has patents pending for IgGs to the following proteins as biomarkers of autoimmune neurological disorders: septin-5, kelch-like protein 11, GFAP, PDE10A, and MAP1B. He works at Mayo Clinic, which offers commercial MOG-IgG and AQP4-IgG testing. He receives no royalties from the sale of tests done at the neuroimmunology Laboratory at Mayo Clinic; Eoin P. Flanagan has served on advisory boards for Alexion, Genentech and Horizon Therapeutics. He has received speaker honoraria from Pharmacy Times. He received royalties from UpToDate. Dr Flanagan was a site primary investigator in a randomized clinical trial on Inebilizumab in neuromyelitis optica spectrum disorder run by Medimmune/Viela-Bio/Horizon Therapeutics. Dr Flanagan has received funding from the NIH (R01NS113828). Dr Flanagan is a member of the medical advisory board of the MOG project. Dr Flanagan is an editorial board member of the Journal of the Neurological Sciences and Neuroimmunology Reports. A patent has been submitted on DACH1-IgG as a biomarker of paraneoplastic autoimmunity.
References
- 1.Banwell B, Bennett JL, Marignier R, et al. Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria. Lancet Neurol. Mar 2023;22(3):268–282. doi: 10.1016/S1474-4422(22)00431-8 [DOI] [PubMed] [Google Scholar]
- 2.Wingerchuk DM, Banwell B, Bennett JL, et al. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology. 2015;85(2):177–189. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Brill L, Ganelin-Cohen E, Dabby R, et al. Age-Related Clinical Presentation of MOG-IgG Seropositivity in Israel. Front Neurol. 2020;11:612304. doi: 10.3389/fneur.2020.612304 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Papp V, Magyari M, Aktas O, et al. Worldwide Incidence and Prevalence of Neuromyelitis Optica: A Systematic Review. Neurology. Jan 12 2021;96(2):59–77. doi: 10.1212/WNL.0000000000011153 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Sechi E, Cacciaguerra L, Chen JJ, et al. Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management. Front Neurol. 2022;13:885218. doi: 10.3389/fneur.2022.885218 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Hor JY, Fujihara K. Epidemiology of myelin oligodendrocyte glycoprotein antibody-associated disease: a review of prevalence and incidence worldwide. Front Neurol. 2023;14:1260358. doi: 10.3389/fneur.2023.1260358 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Akaishi T, Fujimori J, Takahashi T, et al. Seasonal variation of onset in patients with anti-aquaporin-4 antibodies and anti-myelin oligodendrocyte glycoprotein antibody. J Neuroimmunol. Dec 15 2020;349:577431. doi: 10.1016/j.jneuroim.2020.577431 [DOI] [PubMed] [Google Scholar]
- 8.Dos Passos GR, Elsone L, Luppe S, et al. Seasonal distribution of attacks in aquaporin-4 antibody disease and myelin-oligodendrocyte antibody disease. J Neurol Sci. Aug 15 2020;415:116881. doi: 10.1016/j.jns.2020.116881 [DOI] [PubMed] [Google Scholar]
- 9.Orlandi R, Mariotto S, Gajofatto A. Prevalence, incidence, and season distribution of MOG antibody-associated disease in the province of Verona, Italy. Mult Scler Relat Disord. Jul 2022;63:103884. doi: 10.1016/j.msard.2022.103884 [DOI] [PubMed] [Google Scholar]
- 10.Carnero Contentti E, Lopez PA, Pettinicchi JP, et al. Seasonal variation in attacks of neuromyelitis optica spectrum disorders and multiple sclerosis: Evaluation of 794 attacks from a nationwide registry in Argentina. Mult Scler Relat Disord. Feb 2022;58:103466. doi: 10.1016/j.msard.2021.103466 [DOI] [PubMed] [Google Scholar]
- 11.Sechi E, Buciuc M, Pittock SJ, et al. Positive Predictive Value of Myelin Oligodendrocyte Glycoprotein Autoantibody Testing. JAMA Neurol. Jun 1 2021;78(6):741–746. doi: 10.1001/jamaneurol.2021.0912 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Redenbaugh V, Montalvo M, Sechi E, et al. Diagnostic value of aquaporin-4-IgG live cell based assay in neuromyelitis optica spectrum disorders. Mult Scler J Exp Transl Clin. Oct 2021;7(4):20552173211052656. doi: 10.1177/20552173211052656 [DOI] [Google Scholar]
- 13.Flanagan EP, Cabre P, Weinshenker BG, et al. Epidemiology of aquaporin-4 autoimmunity and neuromyelitis optica spectrum. Ann Neurol. May 2016;79(5):775–783. doi: 10.1002/ana.24617 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14.Nytrova P, Dolezal O. Sex bias in multiple sclerosis and neuromyelitis optica spectrum disorders: How it influences clinical course, MRI parameters and prognosis. Front Immunol. 2022;13:933415. doi: 10.3389/fimmu.2022.933415 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Kunchok A, Chen JJ, McKeon A, Mills JR, Flanagan EP, Pittock SJ. Coexistence of Myelin Oligodendrocyte Glycoprotein and Aquaporin-4 Antibodies in Adult and Pediatric Patients. JAMA Neurol. 2020;77(2):257–259. [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
Anonymized study data are available upon reasonable request from the corresponding authors.