Evidence map›Paper›PMID 24804216›Full record

ArticleBioMed research international2014

Inhibitory effects of edaravone in β-amyloid-induced neurotoxicity in rats.

Feng He, Yan-Ping Cao, Feng-Yuan Che, Lian-Hong Yang, Song-Hua Xiao, Jun Liu

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Edaravone alleviates Alzheimer's disease-type pathologies and cognitive deficits.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  10. 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

6 authors at 3 institutions in 1 country.

Feng HeDepartment of Neurology, Linyi People's Hospital, Linyi City, Shandong 276000, China.
Yan-Ping CaoDepartment of Out-Patient, Yulin Teacher's College Hospital, Yulin, Guangxi 537000, China.
Feng-Yuan CheDepartment of Neurology, Linyi People's Hospital, Linyi City, Shandong 276000, China.
Lian-Hong YangDepartment of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangdong 510120, China.
Song-Hua XiaoDepartment of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangdong 510120, China.
Jun LiuDepartment of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangdong 510120, China.ORCID 0000-0001-9202-5878
Sun Yat-sen University · CNLinyi People's Hospital · CNYulin Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyloid protein can damage nerve cells through a variety of biological mechanisms including oxidative stress, alterations in calcium homeostasis, and proapoptosis. Edaravone, a potent free radical scavenger possessing antioxidant effects, has been proved neuroprotective effect in stroke patients. The current study aimed to investigate the effects of EDA in an Aβ-induced rat model of AD, by studying Aβ 1-40-induced voltage-gated calcium channel currents in hippocampal CA1 pyramidal neurons, learning and memory behavioral tests, the number of surviving cholinergic neurons in the basal forebrain, and the acetylcholine level in the hippocampus in this rat model of AD. The results showed that the Aβ 1-40-induced increase of I Ca can be inhibited by EDA in a dose-dependent manner. Treatment with EDA significantly improved Aβ 1-40-induced learning and memory performance. Choline acetyltransferase positive cells in basal forebrain and acetylcholine content in the hippocampus were increased by the administration of EDA as compared with the non-EDA treated Aβ 1-40 group. These results demonstrate that EDA can inhibit the neurotoxic effect of Aβ toxicity. Collectively, these findings suggest that EDA may serve as a potential complemental treatment strategy for AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAntipyrineCA1 Region, HippocampalDisease Models, AnimalEdaravoneFree Radical ScavengersLearningMaleMemoryNeurotoxicity SyndromesPeptide FragmentsRatsRats, Sprague-DawleyAmyloid beta-Peptidesamyloid beta-protein (1-40)AntipyrineEdaravoneFree Radical ScavengersPeptide Fragments

Identifiers

PMID24804216
PMCPMC3996961
OpenAlexW2022129281

What OpenQuestion holds

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LicenceCC BY
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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.