Evidence map›Paper›PMID 31040362›Full record

ArticleScientific reports2019

High dose of dexamethasone protects against EAE-induced motor deficits but impairs learning/memory in C57BL/6 mice.

Nilton Dos Santos, Leonardo S Novaes, Guilherme Dragunas, Jennifer R Rodrigues, Wesley Brandão, Rosana Camarini, Jean Pierre Schatzmann Peron, Carolina Demarchi Munhoz

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-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, 29 citations in OpenAlex.

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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

8 authors at 1 institution in 2 countries.

Nilton Dos SantosDepartment of Pharmacology, Institute of Biomedical Science, University of São Paulo, São Paulo, 05508-000, Brazil.
Leonardo S NovaesDepartment of Pharmacology, Institute of Biomedical Science, University of São Paulo, São Paulo, 05508-000, Brazil.
Guilherme DragunasDepartment of Pharmacology, Institute of Biomedical Science, University of São Paulo, São Paulo, 05508-000, Brazil.
Jennifer R RodriguesDepartment of Pharmacology, Institute of Biomedical Science, University of São Paulo, São Paulo, 05508-000, Brazil.
Wesley BrandãoDepartment of Immunology, Institute of Biomedical Science, University of São Paulo, São Paulo, 05508-000, Brazil.
Rosana CamariniDepartment of Pharmacology, Institute of Biomedical Science, University of São Paulo, São Paulo, 05508-000, Brazil.ORCID http://orcid.org/0000-0002-8131-6108
Jean Pierre Schatzmann PeronDepartment of Immunology, Institute of Biomedical Science, University of São Paulo, São Paulo, 05508-000, Brazil.
Carolina Demarchi MunhozDepartment of Pharmacology, Institute of Biomedical Science, University of São Paulo, São Paulo, 05508-000, Brazil. cdmunhoz@usp.br.ORCID http://orcid.org/0000-0002-8656-5234
Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is an autoimmune and neuroinflammatory disease characterized by demyelination of the Central Nervous System. Immune cells activation and release of pro-inflammatory cytokines play a crucial role in the disease modulation, decisively contributing to the neurodegeneration observed in MS and the experimental autoimmune encephalomyelitis (EAE), the widely used MS animal model. Synthetic glucocorticoids, commonly used to treat the MS attacks, have controversial effects on neuroinflammation and cognition. We sought to verify the influence of dexamethasone (DEX) on the EAE progression and on EAE-induced cognitive deficits. In myelin oligodendrocyte glycoprotein peptide (MOG35-55)-induced EAE female mice, treated once with DEX (50 mg/kg) or not, on the day of immunization, DEX decreased EAE-induced motor clinical scores, infiltrating cells in the spinal cord and delayed serum corticosterone peak. At the asymptomatic phase (8-day post-immunization), DEX did not protected from the EAE-induced memory consolidation deficits, which were accompanied by increased glucocorticoid receptor (GR) activity and decreased EGR-1 expression in the hippocampus. Blunting hippocampal GR genomic activation with DnGR vectors prevented DEX effects on EAE-induced memory impairment. These data suggest that, although DEX improves clinical signs, it decreases cognitive and memory capacity by diminishing neuronal activity and potentiating some aspects of neuroinflammation in EAE.

Indexed as

AnimalsAnti-Inflammatory AgentsCorticosteroneDexamethasoneDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFluorescent Antibody TechniqueHippocampusLearningMemoryMiceMice, Inbred C57BLMotor DisordersMultiple SclerosisReceptors, GlucocorticoidSpinal CordAnti-Inflammatory AgentsCorticosteroneDexamethasoneReceptors, Glucocorticoid

Identifiers

PMID31040362
PMCPMC6491620
OpenAlexW2942967643

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.