Evidence map›Paper›PMID 29869772›Full record

ArticleNeurotoxicity research2018

Protective Effects of Fibroblast Growth Factor 21 Against Amyloid-Beta

Mona Amiri, Nady Braidy, Malihe Aminzadeh

Abstract read
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  11. Review
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  13. Hepatic FGF21: Its Emerging Role in Inter-Organ Crosstalk and Cancers.International journal of biological sciences · 2022
    Review
  14. Article
  15. Physical Exercise-Induced Myokines in Neurodegenerative Diseases.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Review
  18. Inhibition of human amylin aggregation by Flavonoid Chrysin: AnInternational journal of medical sciences · 2021
    Article
  19. Article
  20. 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

3 authors at 3 institutions in 2 countries.

Mona AmiriDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. amiri.mo@tak.iums.ac.ir.
Nady BraidyCentre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Barker Street, Randwick, Sydney, NSW, 2031, Australia. n.braidy@unsw.edu.au.
Malihe AminzadehInstitute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran.
Iran University of Medical Sciences · IRUniversity of Tehran · IRUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the progressive loss of cholinergic neurons. Amyloid beta is a misfolded protein that represents one of the key pathological hallmarks of AD. Numerous studies have shown that Aβ

Indexed as

Amyloid beta-PeptidesAnimalsCaspase 3Cell DeathCell Line, TumorCell SurvivalDose-Response Relationship, DrugFibroblast Growth FactorsHSP90 Heat-Shock ProteinsHumansKlotho ProteinsMembrane ProteinsNeuroblastomaNF-kappa BPeptide FragmentsReactive Oxygen SpeciesAmyloid beta-Peptidesamyloid beta-protein (1-42)Caspase 3fibroblast growth factor 21Fibroblast Growth FactorsHSP90 Heat-Shock ProteinsKLB protein, humanKlotho ProteinsMembrane ProteinsNF-kappa BPeptide FragmentsReactive Oxygen SpeciesReceptors, Fibroblast Growth FactorRNA, Ribosomal, 18SToll-Like Receptor 4Alzheimer’s diseaseAmyloid beta 42FGF21NeuroblastomaNeuroinflammationOxidative stress

Identifiers

PMID29869772
OpenAlexW2883697474

What OpenQuestion holds

Textmetadata
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.