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MOG-IgG (Myelin Oligodendrocyte Glycoprotein Antibody)

Looks for antibodies to MOG, a protein on the coating of nerve fibers; a clear positive can support a MOGAD diagnosis when symptoms fit.

AI-verified against cited sources. Awaiting expert reviewAlso called MOG, MOG-IgG, MOG-AbLOINC 91545-4

What it is

MOG (myelin oligodendrocyte glycoprotein) is a protein on the outer surface of the myelin sheath, the coating that wraps nerve fibers in the brain, optic nerves and spinal cord. In some people the immune system makes antibodies to MOG. The best tests mix your serum with cells that carry MOG and look for antibody binding, which is called a cell-based assay. The result is reported as negative or positive, often with a titer, which is a dilution such as 1:100.

Why it matters

MOG-IgG helps tell MOG antibody-associated disease (MOGAD) from multiple sclerosis and from aquaporin-4 antibody disease after an attack of inflammation in the optic nerve, spinal cord or brain. A positive test alone does not make the diagnosis. Doctors also need a typical attack and must rule out other causes such as multiple sclerosis, and a low-positive result needs extra supporting features. A negative result does not rule out inflammatory nerve disease.

If it’s high

A positive result means MOG antibodies were found. The higher the titer, the more likely it is to be meaningful. In selected clinical groups, the chance that a positive result reflects MOGAD ranges from about 50 to 70% at low titers to near 100% at high titers, depending on the assay and the group. Low-positive results are the least reliable and can occur in people with other conditions, including multiple sclerosis, and in some people without nerve disease. Your neurologist will read the result with your symptoms, your MRI and sometimes a second test.

Common causes

  • A low-positive result that does not reflect MOGAD (seen in some people with multiple sclerosis or other conditions, and in some people without nerve disease)
  • MOG antibody-associated disease (MOGAD), which can cause optic neuritis, transverse myelitis, acute disseminated encephalomyelitis (ADEM) and other brain or brainstem inflammation

What can help

  • Ask which type of assay was used (live or fixed cell-based) and what titer your lab calls a clear positive
  • Ask whether repeating the test with another assay, or testing spinal fluid, would add information
  • Ask your neurologist how your MRI and symptoms fit with this result

What can affect your result

  • Assay type: live or fixed cells, flow cytometry or microscope. Where "positive" starts differs between labs
  • Immune-suppressing treatment before the blood draw can lower antibody levels
  • Titers are not directly comparable between labs, so compare results only with the same lab and method
  • Clinical setting: results are read together with symptoms, MRI and the exclusion of other causes
  • Immune-suppressing treatment can lower antibody levels. Mayo asks that the blood be drawn before such treatment starts, for the best chance of detecting the antibody.
  • Only cell-based assays are accepted for diagnosis. ELISA results do not match cell-based results and are not recommended.
  • Live and fixed cell-based assays can disagree. In one international comparison, a fixed commercial assay missed four clearly positive samples that all seven live assays detected.
  • Low-positive results are the least reproducible. Agreement among live assays was 92% for clearly positive samples but only 28% for low-positive ones.
  • ARUP rejects hemolyzed, contaminated or severely lipemic samples.

Treatment with immune-suppressing medicine can lower antibody levels, and Mayo asks that blood be drawn before it starts. ARUP notes that persistent positivity may be associated with a relapsing course.

When to talk to a clinician

Sudden loss of vision, eye pain with movement, new weakness or numbness, trouble walking, loss of bladder or bowel control, or confusion needs urgent medical attention. Go to an emergency department or call 911 or your local emergency number if these come on suddenly.

Questions you could ask

  • Which type of MOG assay does my lab use, and could a different assay or spinal fluid testing add information?
  • Was AQP4 antibody testing done too?
  • Is my result a clear positive or a low positive on this assay?
  • Do my symptoms and MRI fit with this result, or should we repeat the test with another assay?
  • What changes would tell us to call or come in sooner?

Questions people ask

What does a low-positive MOG-IgG result mean?

A low positive is a weak signal that is less specific. It can be seen in MOGAD, but also in other conditions and in some people without nerve disease. The 2023 criteria need extra evidence from your symptoms and MRI before calling it MOGAD. Your neurologist may repeat the test or use a second assay.

Why do labs report different titers?

Labs use different assays, such as live or fixed cells, and different starting dilutions, so titers are not on one shared scale. A number that is a clear positive on one assay may be low on another. Compare results only with the same lab and method.

Can I have MOGAD with a negative blood test?

It is possible. ARUP notes that a negative test does not rule out an inflammatory nerve disease. In people with a strong clinical picture, doctors sometimes repeat the test with a different assay or test spinal fluid.

Show the science and sources

For clinicians and researchers

MOG-IgG is detected by cell-based assays (CBA) using cells that express full-length human MOG. Assays may be live or fixed, and read by microscope (CBA-IFA, as at ARUP) or flow cytometry (as in Mayo's IgG1 FACS assay). The 2023 International MOGAD Panel criteria require a compatible core demyelinating event, exclusion of better alternative diagnoses such as multiple sclerosis, and a positive MOG-IgG by CBA. A clear positive is a fixed-CBA serum titer of 1:100 or more, or an assay-specific live-CBA definition such as at least two doubling dilutions above the cutoff. A low positive is a fixed-CBA titer of at least 1:10 but under 1:100, or the low-positive range of a validated live CBA, and it requires AQP4-IgG seronegativity plus at least one supporting clinical or MRI feature. Positive results without a titer and isolated CSF positivity carry the same added requirements as low positive. Fc- or IgG1-specific secondary antibodies are preferred, and anti-IgG (H+L) detection is accepted in externally validated in-house assays. ELISA does not correlate with CBA and is not accepted. In a blinded comparison, agreement among live CBAs was 92% for clearly positive samples and only 28% for low-positive samples, and positive predictive value in selected cohorts runs from about 50 to 70% at low titers to near 100% at high titers. ARUP's screen is positive from a titer of 1:10, with a reflex titer. Mayo's screen is reported as negative or positive with a reflex titer. Estimated incidence is 1.6 to 3.4 per million per year and prevalence about 20 per million.

LOINC 91545-4 (primary), 91544-7, 90248-6, 84873-9. Specimen: serum.

Sources

  1. Myelin Oligodendrocyte Glycoprotein (MOG) Antibody, IgG by CBA-IFA With Reflex to Titer, Serum (ARUP test 3001277), ARUP Laboratories (2026)
  2. Myelin Oligodendrocyte Glycoprotein (MOG-IgG1) Fluorescence-Activated Cell Sorting (FACS) Assay, Serum (Mayo Clinic Laboratories test MOGFS), Mayo Clinic Laboratories (Extended Catalog mirror, testcatalog.org) (2026)
  3. Beyond Positivity: Understanding and Interpreting MOG-IgG Testing in MOGAD, Journal of Clinical Neurology 2026;22:501-513 (2026)
  4. Ongoing Challenges in the Diagnosis of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease, JAMA Neurology 2023;80:1377-1379 (2023)
  5. Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria, The Lancet Neurology 2023;22:268-282 (2023)
  6. LOINC codes verified with the NLM Clinical Tables LOINC search (e.g. 91544-7), U.S. National Library of Medicine

AI-verified against cited sources. Awaiting expert review. Last reviewed 2026-10-03. How we build and check these pages.

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