Evidence map›Paper›PMID 32388602›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2020

Novel NMDA-receptor antagonists ameliorate vanadium neurotoxicity.

A D Ladagu, F E Olopade, O R Folarin, T O Elufioye, J V Wallach, M B Dybek, J O Olopade, A Adejare

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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2020. 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
0.8field-weighted citation impact, top 32% 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

8 authors at 2 institutions in 2 countries.

A D LadaguDepartment of Veterinary Anatomy, University of Ibadan, Oyo, Nigeria.
F E OlopadeDepartment of Anatomy, University of Ibadan, Oyo, Nigeria.
O R FolarinDepartment of Veterinary Anatomy, University of Ibadan, Oyo, Nigeria.
T O ElufioyeDepartment of Pharmacognosy, University of Ibadan, Oyo, Nigeria.
J V WallachDepartment of Pharmaceutical Sciences, Philadelphia College of Pharmacy, University of the Sciences, Philadelphia, PA, USA.
M B DybekDepartment of Pharmaceutical Sciences, Philadelphia College of Pharmacy, University of the Sciences, Philadelphia, PA, USA.
J O OlopadeDepartment of Veterinary Anatomy, University of Ibadan, Oyo, Nigeria. jkayodeolopade@yahoo.com.ORCID 0000-0002-3470-0801
A AdejareDepartment of Pharmaceutical Sciences, Philadelphia College of Pharmacy, University of the Sciences, Philadelphia, PA, USA.
University of Ibadan · NGUniversity of the Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Various NMDA-receptor antagonists have been investigated for their therapeutic potential in Alzheimer's disease with memantine shown to be safe and with relative efficacy. There is, however, need to develop novel drugs to counter tolerance and with better efficacy in ameliorating neurodegeneration. We have shown neurodegeneration in different models of vanadium-exposed mice. This study was designed to evaluate and ascertain the potency of three novel NMDA-receptor antagonists (Compounds A, B and C) to ameliorate neurodegeneration in vanadium-exposed mice. One-month-old mice (n = 6) received sterile water (control) and another group (n = 6) was treated with vanadium (3 mg/kg sodium metavanadate) intraperitoneally for 1 month. Three other groups (n = 6) received vanadium and compounds A, B and C (4.35 mg/kg, 30 mg/kg and 100 mg/kg, respectively) simultaneously for the same period. Assessment of pathologies and neurodegeneration in different brain regions was done to test the ameliorative effects of the 3 antagonists using different immunohistochemical markers. Vanadium exposure resulted in reduced calbindin expression and pyknosis of Purkinje cells, cell loss and destruction of apical dendrites with greater percentage of cytoplasmic vacuolations, morphological alterations characterized by cell clustering and multiple layering patterns in the Purkinje cell layer. In addition, the observed degeneration included demyelination, increased GFAP-immunoreactive cells and microgliosis. Simultaneous administration of the compounds to vanadium-exposed mice resulted in the preservation of cellular integrity in the same anatomical regions and restoration of the cells' vitality with reduced astroglial and microglial activation.

Indexed as

Nerve DegenerationAnimalsAstrocytesCalbindinsCell DeathDisease Models, AnimalExcitatory Amino Acid AntagonistsGlial Fibrillary Acidic ProteinMiceMicrogliaNeurotoxicity SyndromesPurkinje CellsReceptors, N-Methyl-D-AspartateVanadatesCalbindinsExcitatory Amino Acid AntagonistsGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseReceptors, N-Methyl-D-AspartateVanadatesAlzheimer’s diseaseCompoundsNeurodegenerationNMDA-receptor antagonistPurkinje cellsVanadium

Identifiers

PMID32388602
OpenAlexW3023903585

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.