Evidence map›Paper›PMID 30858445›Full record

ArticleScientific reports2019

Cognitive impairment in an animal model of multiple sclerosis and its amelioration by glatiramer acetate.

Rina Aharoni, Nofar Schottlender, Dekel D Bar-Lev, Raya Eilam, Michael Sela, Michael Tsoory, Ruth Arnon

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
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  6. Pharmaceuticals (Basel, Switzerland) · 2024
    Article
  7. Electrical stimulation of the vagus nerve ameliorates inflammation and disease activity in a rat EAE model of multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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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

7 authors at 1 institution in 1 country.

Rina AharoniDepartment of Immunology, The Weizmann Institute of Science, Rehovot, 761001, Israel. rina.aharoni@weizmann.ac.il.
Nofar SchottlenderDepartment of Immunology, The Weizmann Institute of Science, Rehovot, 761001, Israel.
Dekel D Bar-LevDepartment of Immunology, The Weizmann Institute of Science, Rehovot, 761001, Israel.
Raya EilamDepartment of Veterinary Resources, The Weizmann Institute of Science, Rehovot, 761001, Israel.
Michael SelaDepartment of Immunology, The Weizmann Institute of Science, Rehovot, 761001, Israel.
Michael TsooryDepartment of Veterinary Resources, The Weizmann Institute of Science, Rehovot, 761001, Israel.
Ruth ArnonDepartment of Immunology, The Weizmann Institute of Science, Rehovot, 761001, Israel. ruth.arnon@weizmann.ac.il.
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The severe motor impairment in the MS animal model experimental autoimmune encephalomyelitis (EAE) obstructs the assessment of cognitive functions. We developed an experimental system that evaluates memory faculties in EAE-affected mice, irrespective of their motor performance, enabling the assessment of cognitive impairments along the disease duration, the associated brain damage, and the consequences of glatiramer acetate (GA) treatment on these manifestations. The delayed-non-matching to sample (DNMS) T-maze task, testing working and long term memory was adapted and utilized. Following the appearance of clinical manifestations task performances of the EAE-untreated mice drastically declined. Cognitive impairments were associated with disease severity, as indicated by a significant correlation between the T-maze performance and the clinical symptoms in EAE-untreated mice. GA-treatment conserved cognitive functions, so that despite their exhibited mild motor impairments, the treated mice performed similarly to naïve controls. The cognitive deficit of EAE-mice coincided with inflammatory and neurodegenerative damage to the frontal cortex and the hippocampus; these damages were alleviated by GA-treatment. These combined findings indicate that in addition to motor impairment, EAE leads to substantial impairment of cognitive functions, starting at the early stages and increasing with disease aggravation. GA-treatment, conserves cognitive capacities and prevents its disease related deterioration.

Indexed as

CognitionAnimalsAnti-Inflammatory AgentsEncephalomyelitis, Autoimmune, ExperimentalFrontal LobeGlatiramer AcetateHippocampusMaze LearningMiceMice, Inbred C57BLMovementNeuroprotective AgentsAnti-Inflammatory AgentsGlatiramer AcetateNeuroprotective Agents

Identifiers

PMID30858445
PMCPMC6412002
OpenAlexW2922360167

What OpenQuestion holds

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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.