Evidence map›Paper›PMID 28796815›Full record

ArticlePloS one2017

Effect of teriflunomide on cortex-basal ganglia-thalamus (CxBGTh) circuit glutamatergic dysregulation in the Theiler's Murine Encephalomyelitis Virus mouse model of multiple sclerosis.

Claire M Modica, Ferdinand Schweser, Michelle L Sudyn, Nicola Bertolino, Marilena Preda, Paul Polak, Danielle M Siebert, Jacqueline C Krawiecki, Michele Sveinsson, Jesper Hagemeier and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 13 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

13 authors at 2 institutions in 1 country.

Claire M ModicaNeuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Ferdinand SchweserDepartment of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Michelle L SudynNeuroscience Program, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Nicola BertolinoDepartment of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Marilena PredaDepartment of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Paul PolakDepartment of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Danielle M SiebertDepartment of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Jacqueline C KrawieckiDepartment of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Michele SveinssonDepartment of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Jesper HagemeierDepartment of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Michael G DwyerDepartment of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Suyog PolDepartment of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.
Robert ZivadinovDepartment of Neurology, Buffalo Neuroimaging Analysis Center, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, United States of America.ORCID http://orcid.org/0000-0002-7799-1485
University at Buffalo, State University of New York · USImaging Center · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
University of Buffalo Clinical and Translational Science Institute - Supplement SchulyerUL1TR001412 · NCATS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI MURPHY, TIMOTHY F · 2015 to 2024
$33.8M
NCATS NIH HHS UL1 TR001412NCI NIH HHS P30 CA016056
6 · The paper itself

Abstract

backgroundPathology of gray matter is associated with development of physical and cognitive disability in patients with multiple sclerosis. In particular, glutamatergic dysregulation in the cortex-basal ganglia-thalamus (CxBGTh) circuit could be associated with decline in these behaviors.

objectivesTo investigate the effect of an immunomodulatory therapy (teriflunomide, Aubagio®) on changes of the CxBGTh loop in the Theiler's Murine Encephalomyelitis Virus, (TMEV) mouse model of MS.

methodsForty-eight (48) mice were infected with TMEV, treated with teriflunomide (24) or control vehicle (24) and followed for 39 weeks. Mice were examined with MRS and volumetric MRI scans (0, 8, 26, and 39 weeks) in the cortex, basal ganglia and thalamus, using a 9.4T scanner, and with behavioral tests (0, 4, 8, 12, 17, 26, and 39 weeks). Within conditions, MRI measures were compared between two time points by paired samples t-test and across multiple time points by repeated measures ANOVA (rmANOVA), and between conditions by independent samples t-test and rmANOVA, respectively. Data were considered as significant at the p<0.01 level and as a trend at p<0.05 level.

resultsIn the thalamus, the teriflunomide arm exhibited trends toward decreased glutamate levels at 8 and 26 weeks compared to the control arm (p = 0.039 and p = 0.026), while the control arm exhibited a trend toward increased glutamate between 0 to 8 weeks (p = 0.045). In the basal ganglia, the teriflunomide arm exhibited a trend toward decreased glutamate earlier than the control arm, from 0 to 8 weeks (p = 0.011), resulting in decreased glutamate compared to the control arm at 8 weeks (p = 0.016).

conclusionsTeriflunomide may reduce possible excitotoxicity in the thalamus and basal ganglia by lowering glutamate levels.

Indexed as

AnimalsBasal GangliaCell LineCorpus CallosumCrotonatesDisease Models, AnimalDrug Evaluation, PreclinicalExcitatory Amino Acid AgentsFemalegamma-Aminobutyric AcidGlutamic AcidHydroxybutyratesMesocricetusMiceMultiple SclerosisMyelitisCrotonatesExcitatory Amino Acid Agentsgamma-Aminobutyric AcidGlutamic AcidHydroxybutyratesNitrilesteriflunomideToluidines

Identifiers

PMID28796815
PMCPMC5552032
OpenAlexW2742705326

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.