Evidence map›Paper›PMID 26207848›Full record

ArticleBrain pathology (Zurich, Switzerland)2016

A New Targeted Model of Experimental Autoimmune Encephalomyelitis in the Common Marmoset.

Ruth Martha Stassart, Gunther Helms, Enrique Garea-Rodríguez, Stefan Nessler, Liat Hayardeny, Christiane Wegner, Christina Schlumbohm, Eberhard Fuchs, Wolfgang Brück

Open access · bronzeAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Neurodegeneration in multiple sclerosis.WIREs mechanisms of disease · 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

9 authors at 4 institutions in 2 countries.

Ruth Martha StassartInstitute of Neuropathology, University Medical Center, Georg-August-University Göttingen, Göttingen, Germany.
Gunther HelmsDepartment of Cognitive Neurology, University Medical Center, Georg-August-University Göttingen, Göttingen, Germany.
Enrique Garea-RodríguezDepartment of Neuroanatomy, Institute of Anatomy and Cell Biology, Albert-Ludwigs-University Freiburg, Freiburg, Germany.
Stefan NesslerInstitute of Neuropathology, University Medical Center, Georg-August-University Göttingen, Göttingen, Germany.
Liat HayardenyTeva Pharmaceutical Industries, Netanya, Israel.
Christiane WegnerInstitute of Neuropathology, University Medical Center, Georg-August-University Göttingen, Göttingen, Germany.
Christina SchlumbohmClinical Neurobiology Laboratory, German Primate Center, Göttingen, Germany.
Eberhard FuchsClinical Neurobiology Laboratory, German Primate Center, Göttingen, Germany.
Wolfgang BrückInstitute of Neuropathology, University Medical Center, Georg-August-University Göttingen, Göttingen, Germany.
University of Göttingen · DEGerman Primate Center · DETeva Pharmaceuticals (Israel) · ILUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is the most common cause for sustained disability in young adults, yet treatment options remain very limited. Although numerous therapeutic approaches have been effective in rodent models of experimental autoimmune encephalomyelitis (EAE), only few proved to be beneficial in patients with MS. Hence, there is a strong need for more predictive animal models. Within the past decade, EAE in the common marmoset evolved as a potent, alternative model for MS, with immunological and pathological features resembling more closely the human disease. However, an often very rapid and severe disease course hampers its implementation for systematic testing of new treatment strategies. We here developed a new focal model of EAE in the common marmoset, induced by myelin oligodendrocyte glycoprotein (MOG) immunization and stereotactic injections of proinflammatory cytokines. At the injection site of cytokines, confluent inflammatory demyelinating lesions developed that strongly resembled human MS lesions. In a proof-of-principle treatment study with the immunomodulatory compound laquinimod, we demonstrate that targeted EAE in marmosets provides a promising and valid tool for preclinical experimental treatment trials in MS research.

Indexed as

CallithrixEncephalomyelitis, Autoimmune, ExperimentalAnimalsCytokinesFemaleMaleMyelin-Oligodendrocyte GlycoproteinCytokinesMyelin-Oligodendrocyte Glycoproteincommon marmosetdemyelinationexperimental autoimmune encephalomyelitisimmunomodulationlaquinimodmultiple sclerosis

Identifiers

PMID26207848
PMCPMC8029260
OpenAlexW2159831122

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.