Evidence map›Paper›PMID 36732292›Full record

ArticleBrain : a journal of neurology2023

Cerebrospinal fluid immunoglobulins in primary progressive multiple sclerosis are pathogenic.

Jamie K Wong, Jerry Lin, Nathan J Kung, Alexandra L Tse, Serena J E Shimshak, Anna K Roselle, Francesca M Cali, Jessie Huang, Joseph M Beaty, Taylor M Shue and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Brain : a journal of neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  6. Central TYK2 inhibition identifies TYK2 as a key neuroimmune modulator.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Jamie K WongTisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.ORCID 0000-0002-9059-0053
Jerry LinTisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.
Nathan J KungTisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.
Alexandra L TseTisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.
Serena J E ShimshakTisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.
Anna K RoselleTisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.
Francesca M CaliTisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.
Jessie HuangTisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.
Joseph M BeatyTisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.
Taylor M ShueTisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.
Saud A SadiqTisch Multiple Sclerosis Research Center of New York, New York, NY 10019, USA.
Tisch Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis is clinically characterized by relapses and remissions (relapsing-remitting multiple sclerosis) that over time may evolve to a progressive course (secondary progressive multiple sclerosis) or as having a progressive course from disease onset (primary progressive multiple sclerosis). At present, it is not definitively known whether these clinical entities constitute a single pathological disease or whether these manifestations represent two distinct disease entities sharing inflammatory demyelination as a pathological feature. Here we show using a novel mouse model that CSF of primary progressive multiple sclerosis patients is unique in its capacity to induce motor disability and spinal cord pathology including demyelination, impaired remyelination, reactive astrogliosis and axonal damage. Notably, removal of immunoglobulin G from primary progressive multiple sclerosis CSF via filtration or immunodepletion attenuates its pathogenic capacity. Furthermore, injection of recombinant antibodies derived from primary progressive multiple sclerosis CSF recapitulates the pathology. Our findings suggest that the clinical and pathological features of primary progressive multiple sclerosis are antibody-mediated and pathogenically distinct from relapsing-remitting and secondary progressive multiple sclerosis. Our study has potentially important implications for the development of specific therapies for patients with primary progressive multiple sclerosis.

Indexed as

Motor DisordersMultiple SclerosisMultiple Sclerosis, Chronic ProgressiveMultiple Sclerosis, Relapsing-RemittingPersons with DisabilitiesAnimalsCerebrospinal FluidDisease ProgressionHumansImmunoglobulin GMiceImmunoglobulin GantibodiesCSFprimary progressive multiple sclerosis

Identifiers

PMID36732292
PMCPMC10151187
OpenAlexW4318937785

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.