Evidence map›Paper›PMID 30266776›Full record

ArticleEMBO molecular medicine2018

Early auto-immune targeting of photoreceptor ribbon synapses in mouse models of multiple sclerosis.

Mayur Dembla, Ajay Kesharwani, Sivaraman Natarajan, Claudia Fecher-Trost, Richard Fairless, Sarah K Williams, Veit Flockerzi, Ricarda Diem, Karin Schwarz, Frank Schmitz

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

27 citing papers in PubMed, 32 citations in OpenAlex.

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  14. Synapse Dysfunctions in Multiple Sclerosis.International journal of molecular sciences · 2023
    Review
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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

10 authors at 2 institutions in 1 country.

Mayur DemblaDepartment of Neuroanatomy, Institute of Anatomy and Cell Biology, Medical School, Saarland University, Homburg, Germany dotdot.mayur@gmail.com Karin.Schwarz@uks.eu frank.schmitz@uks.eu.ORCID 0000-0002-0912-6828
Ajay KesharwaniDepartment of Neuroanatomy, Institute of Anatomy and Cell Biology, Medical School, Saarland University, Homburg, Germany.
Sivaraman NatarajanDepartment of Neuroanatomy, Institute of Anatomy and Cell Biology, Medical School, Saarland University, Homburg, Germany.
Claudia Fecher-TrostInstitute of Experimental and Clinical Pharmacology and Toxicology, Medical School, Saarland University, Homburg, Germany.
Richard FairlessDepartment of Neurology, University Clinic Heidelberg, Heidelberg, Germany.
Sarah K WilliamsDepartment of Neurology, University Clinic Heidelberg, Heidelberg, Germany.
Veit FlockerziInstitute of Experimental and Clinical Pharmacology and Toxicology, Medical School, Saarland University, Homburg, Germany.
Ricarda DiemDepartment of Neurology, University Clinic Heidelberg, Heidelberg, Germany.
Karin SchwarzDepartment of Neuroanatomy, Institute of Anatomy and Cell Biology, Medical School, Saarland University, Homburg, Germany dotdot.mayur@gmail.com Karin.Schwarz@uks.eu frank.schmitz@uks.eu.ORCID 0000-0002-7328-1427
Frank SchmitzDepartment of Neuroanatomy, Institute of Anatomy and Cell Biology, Medical School, Saarland University, Homburg, Germany dotdot.mayur@gmail.com Karin.Schwarz@uks.eu frank.schmitz@uks.eu.ORCID 0000-0003-1457-6222
Saarland University · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Optic neuritis is one of the first manifestations of multiple sclerosis. Its pathogenesis is incompletely understood, but considered to be initiated by an auto-immune response directed against myelin sheaths of the optic nerve. Here, we demonstrate in two frequently used and well-validated mouse models of optic neuritis that ribbon synapses in the myelin-free retina are targeted by an auto-reactive immune system even before alterations in the optic nerve have developed. The auto-immune response is directed against two adhesion proteins (CASPR1/CNTN1) that are present both in the paranodal region of myelinated nerves as well as at retinal ribbon synapses. This occurs in parallel with altered synaptic vesicle cycling in retinal ribbon synapses and altered visual behavior before the onset of optic nerve demyelination. These findings indicate that early synaptic dysfunctions in the retina contribute to the pathology of optic neuritis in multiple sclerosis.

Indexed as

AutoimmunityAnimalsAntibodiesCattleComplement ActivationContactin 1Disease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalHEK293 CellsHumansMice, Inbred C57BLMultiple SclerosisOptic NerveOptic NeuritisPhotoreceptor Cells, VertebrateRetinaAntibodiesCntn1 protein, mouseContactin 1CASPR1multiple sclerosisretinaribbon synapseRIBEYE

Identifiers

PMID30266776
PMCPMC6220320
OpenAlexW2894186076

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.