Evidence map›Paper›PMID 31728886›Full record

ArticleMetabolic brain disease2020

IFNG/IFNG-AS1 expression level balance: implications for autism spectrum disorder.

Hamid Fallah, Arezou Sayad, Fatemeh Ranjbaran, Fatemeh Talebian, Soudeh Ghafouri-Fard, Mohammad Taheri

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Article in Metabolic brain disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Emerging Role of Non-coding RNAs in Autism Spectrum Disorder.Journal of molecular neuroscience : MN · 2022
    Review
  11. Review
  12. Decoding LncRNAs.Cancers · 2021
    Review
  13. Review
  14. 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 2 countries.

Hamid FallahDepartment of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Arezou SayadDepartment of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran. ar.sayad@yahoo.com.
Fatemeh RanjbaranIran University of Medical Sciences, Tehran, Iran.
Fatemeh TalebianOhio State University Medical Center, Columbus, OH, USA.
Soudeh Ghafouri-FardDepartment of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohammad TaheriDepartment of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Mohammad_823@yahoo.com.
Shahid Beheshti University of Medical Sciences · IRIran University of Medical Sciences · IRThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder associated with different epidemiological, genetic, epigenetic, and environmental factors. Although its etiology is not fully understood, immune dysfunction is implicated in this disease. Recently, a large number of genes encoding long noncoding RNAs (lncRNAs) were discovered which act as positive or negative regulators of neighboring target genes. The lncRNA, Interferon gamma-antisense RNA (IFNG-AS1), regulates expression levels of the Interferon gamma (IFNG) gene. In the present study, we investigated expression of IFNG and IFNG-AS1 in 50 children with ASD (15 females and 35 males, mean age: 6 ± 1.4 years) and 50 healthy controls (14 females and 36 males, mean age: 6 ± 1.74 years) by real time PCR technique. The results showed significant up-regulation of IFNG and down-regulation of IFNG-AS1 expression in children with ASD compared to controls (Fold change = 1.5, P < 0.0001; Fold change = -0.143, P = 0.013, respectively). The IFNG expression level increase was more pronounced in male ASD children (Fold change = 1.621; p < 0.0001). Our data reveal a functional disruption in the interactive network of IFNG/IFNG-AS1 regulation, which could be a contributing factor in the chronic inflammatory aspect of ASD. Our findings can help understanding the underlying contributors to ASD pathogenesis and find novel treatment options for children with ASD.

Indexed as

Autism Spectrum DisorderCase-Control StudiesChildFemaleGene ExpressionHumansInterferon-gammaMaleRNA, Long NoncodingIFNG protein, humanInterferon-gammaRNA, Long NoncodingAutism spectrum disorder (ASD)INFGINFG-AS1

Identifiers

PMID31728886
OpenAlexW2986345677

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.