Evidence map›Paper›PMID 25635259›Full record

ReviewNeurology(R) neuroimmunology & neuroinflammation2015

Does MOG Ig-positive AQP4-seronegative opticospinal inflammatory disease justify a diagnosis of NMO spectrum disorder?

Scott S Zamvil, Anthony J Slavin

Open access · goldAbstract readReview
In one paragraph

Review in Neurology(R) neuroimmunology & neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 2 pooled it
29.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

142 citing papers in PubMed, 2 syntheses or guidelines pooled it, 270 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Ten Years ofNeurology(R) neuroimmunology & neuroinflammation · 2025
    Article
  7. NMOSD and MOGAD: an evolving disease spectrum.Nature reviews. Neurology · 2024
    Review
  8. MOG CNS Autoimmunity and MOGAD.Neurology(R) neuroimmunology & neuroinflammation · 2024
    Review
  9. Should We Measure CSF Complement Levels in Patients With MOGAD?Neurology(R) neuroimmunology & neuroinflammation · 2024
    Article
  10. Life-Threatening MOG Antibody-Associated Hemorrhagic ADEM With Elevated CSF IL-6.Neurology(R) neuroimmunology & neuroinflammation · 2024
    Article
  11. Article
  12. Article
  13. Thermodynamics andThe journal of physical chemistry. B · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. T cell deletional tolerance restricts AQP4 but not MOG CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Article
  20. Article

82 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Scott S ZamvilDepartment of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco; and Abbvie Bioresearch Center Inc. (A.J.S.), Worcester, MA.
Anthony J SlavinDepartment of Neurology and Program in Immunology (S.S.Z.), University of California, San Francisco; and Abbvie Bioresearch Center Inc. (A.J.S.), Worcester, MA.
AbbVie (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While neuromyelitis optica (NMO) immunoglobulin (Ig) G is considered the hallmark serologic marker of NMO, its association is not absolute, as NMO IgG is not detected in approximately one-fourth of the patients diagnosed with NMO spectrum disorder (NMOSD). Thus, the recent discovery that antibodies to myelin oligodendrocyte glycoprotein (MOG) are detected in some NMO IgG-seronegative patients manifesting clinical and neuroimaging signs of NMO or NMOSD has created tremendous excitement. However, it may be premature to classify this subgroup as NMOSD. NMO is considered an autoimmune astrocytopathy, and aquaporin-4 (AQP4), expressed on astrocytes, is recognized as the target autoantigen of NMO IgG. As its name denotes, MOG is produced by oligodendrocytes, CNS myelin-producing cells, and MOG is well-recognized as one of the candidate autoantigens in multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADEM). Thus, is it possible that the clinical NMOSD-like phenotype associated with MOG-specific antibodies represents a variant of opticospinal MS or ADEM but not AQP4 autoimmunity or NMOSD? Whether this MOG-Ig positive AQP4-seronegative phenotype should be classified as NMOSD, opticospinal MS, or a unique entity is not simply a theoretical question but rather has practical implications for patients, their physicians, insurance carriers, and clinical investigators conducting NMO treatment trials.

Identifiers

PMID25635259
PMCPMC4309526
OpenAlexW2162576364

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.