Evidence map›Paper›PMID 34768760›Full record

ArticleInternational journal of molecular sciences2021

Memantine Modulates Oxidative Stress in the Rat Brain following Experimental Autoimmune Encephalomyelitis.

Beata Dąbrowska-Bouta, Lidia Strużyńska, Marta Sidoryk-Węgrzynowicz, Grzegorz Sulkowski

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Modulating glutamate neurotransmission inFrontiers in immunology · 2026
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  17. Neurodegenerative Diseases: From Molecular Basis to Therapy.International journal of molecular sciences · 2022
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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

4 authors at 1 institution in 1 country.

Beata Dąbrowska-BoutaLaboratory of Pathoneurochemistry, Department of Neurochemistry, Mossakowski Medical Research Institute, Polish Academy of Sciences, 5 Pawińskiego Str., 02-106 Warsaw, Poland.
Lidia StrużyńskaLaboratory of Pathoneurochemistry, Department of Neurochemistry, Mossakowski Medical Research Institute, Polish Academy of Sciences, 5 Pawińskiego Str., 02-106 Warsaw, Poland.
Marta Sidoryk-WęgrzynowiczLaboratory of Pathoneurochemistry, Department of Neurochemistry, Mossakowski Medical Research Institute, Polish Academy of Sciences, 5 Pawińskiego Str., 02-106 Warsaw, Poland.ORCID 0000-0003-3916-7660
Grzegorz SulkowskiLaboratory of Pathoneurochemistry, Department of Neurochemistry, Mossakowski Medical Research Institute, Polish Academy of Sciences, 5 Pawińskiego Str., 02-106 Warsaw, Poland.ORCID 0000-0002-4812-2205
Polish Academy of Sciences · PL

Funding

Mossakowski Medical Research Centre This manuscript is financed from the statutable funds provided by the Ministry of Education and Science for Mossakowski Medical Research Institute Polish Academy of Sciences, Warsaw, Poland (9/2021).
6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE) is an animal model most commonly used in research on the pathomechanisms of multiple sclerosis (MS). The inflammatory processes, glutamate excitotoxicity, and oxidative stress have been proposed as determinants accompanying demyelination and neuronal degeneration during the course of MS/EAE. The aim of the current study was to characterize the role of NMDA receptors in the induction of oxidative stress during the course of EAE. The effect of memantine, the uncompetitive NMDA receptor antagonist, on modulation of neurological deficits and oxidative stress in EAE rats was analyzed using several experimental approaches. We demonstrated that the expression of antioxidative enzymes (superoxide dismutases SOD1 and SOD2) were elevated in EAE rat brains. Under the same experimental conditions, we observed alterations in oxidative stress markers such as increased levels of malondialdehyde (MDA) and decreased levels of sulfhydryl (-SH) groups, both protein and non-protein (indicating protein damage), and a decline in reduced glutathione. Importantly, pharmacological inhibition of ionotropic NMDA glutamate receptors by their antagonist memantine improved the physical activity of EAE rats, alleviated neurological deficits such as paralysis of tail and hind limbs, and modulated oxidative stress parameters (MDA, -SH groups, SOD's). Furthermore, the current therapy aiming to suppress NMDAR-induced oxidative stress was partially effective when NMDAR's antagonist was administered at an early (asymptomatic) stage of EAE.

Indexed as

AnimalsBody WeightBrainEncephalomyelitis, Autoimmune, ExperimentalExcitatory Amino Acid AntagonistsFemaleMemantineNervous System DiseasesOxidative StressRatsRats, Inbred LewReceptors, N-Methyl-D-AspartateSuperoxide DismutaseThiobarbituric Acid Reactive SubstancesExcitatory Amino Acid AntagonistsMemantineReceptors, N-Methyl-D-AspartateSuperoxide DismutaseThiobarbituric Acid Reactive SubstancesEAEexcitotoxicityglutamate receptor antagonistoxidative stress-SH groupssuperoxide dismutase

Identifiers

PMID34768760
PMCPMC8583197
OpenAlexW3207518338

What OpenQuestion holds

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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.