Evidence map›Paper›PMID 29096633›Full record

ArticleMalaria journal2017

Cerebral malaria induces electrophysiological and neurochemical impairment in mice retinal tissue: possible effect on glutathione and glutamatergic system.

Karen R H M Oliveira, Nayara Kauffmann, Luana K R Leão, Adelaide C F Passos, Fernando A F Rocha, Anderson M Herculano, José L M do Nascimento

Open access · goldAbstract read
In one paragraph

Article in Malaria journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Non-cerebral malaria: does such a thing exist?Memorias do Instituto Oswaldo Cruz · 2025
    Review
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  9. Melatonin Prevents Brain Damage and Neurocognitive Impairment Induced byFrontiers in cellular and infection microbiology · 2020
    Article
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.

Karen R H M OliveiraLaboratório de Neurofarmacologia Experimental, Instituto de Ciências Biológicas, Universidade Federal do Pará, R. Augusto Corrêa, 01, Belém, PA, 66075-110, Brazil. karenrenata@yahoo.com.br.
Nayara KauffmannLaboratório de Neurofarmacologia Experimental, Instituto de Ciências Biológicas, Universidade Federal do Pará, R. Augusto Corrêa, 01, Belém, PA, 66075-110, Brazil.
Luana K R LeãoLaboratório de Neurofarmacologia Experimental, Instituto de Ciências Biológicas, Universidade Federal do Pará, R. Augusto Corrêa, 01, Belém, PA, 66075-110, Brazil.
Adelaide C F PassosLaboratório de Neurofarmacologia Experimental, Instituto de Ciências Biológicas, Universidade Federal do Pará, R. Augusto Corrêa, 01, Belém, PA, 66075-110, Brazil.
Fernando A F RochaLaboratório de Neurofisiologia Eduardo Oswaldo Cruz, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, Pará, Brazil.
Anderson M HerculanoLaboratório de Neurofarmacologia Experimental, Instituto de Ciências Biológicas, Universidade Federal do Pará, R. Augusto Corrêa, 01, Belém, PA, 66075-110, Brazil.
José L M do NascimentoLaboratório de Neuroquímica Molecular e Celular Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, Pará, Brazil.
Universidade Federal do Pará · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCerebral malaria (CM) is a severe complication resulting from Plasmodium falciparum infection. This condition has usually been associated with cognitive, behavioural and motor dysfunctions, being the retinopathy the most serious consequence resulting from the disease. The pathophysiological mechanisms underlying this complication remain incompletely understood. Several experimental models of CM have already been developed in order to clarify those mechanisms related to this syndrome. In this context, the present work has been performed to investigate which possible electrophysiological and neurochemistry alterations could be involved in the CM pathology.

methodsExperimental CM was induced in Plasmodium berghei-infected male and female C57Bl/6 mice. The survival and neurological symptoms of CM were registered. Brains and retina were assayed for TNF levels and NOS2 expression. Electroretinography measurements were recorded to assessed a- and b-wave amplitudes and neurochemicals changes were evaluated by determination of glutamate and glutathione levels by HPLC.

resultsSusceptible C57Bl/6 mice infected with ≈ 10

conclusionsIn summary, these findings indicate for the first time that CM induces neurochemical and electrophysiological impairment in the mice retinal tissue, in a TNF-independent manner.

Indexed as

AnimalsFemaleGlutamic AcidGlutathioneMalaria, CerebralMaleMiceMice, Inbred C57BLPlasmodium bergheiRetinaRetinal Cone Photoreceptor CellsRetinal DiseasesGlutamic AcidGlutathioneCerebral malariaElectroretinogram and cone photoreceptor responseGlutamate uptakeGlutathione

Identifiers

PMID29096633
PMCPMC5668953
OpenAlexW2766996433

What Socratic 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 Socratic graph.