Evidence map›Paper›PMID 30415889›Full record

Trial reportEBioMedicine2018

Neuregulin1 types mRNA level changes in autism spectrum disorder, and is associated with deficit in executive functions.

Samane Abbasy, Fazlollah Shahraki, Arvin Haghighatfard, Masoume Ghasemzadeh Qazvini, Sahel Towfigh Rafiei, Elnaz Noshadirad, Mahdi Farhadi, Horie Rezvani Asl, Atena Alsadat Shiryazdi, Rana Ghamari and 17 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. The Ambiguous Role of Growth Factors in Autism: What Do We Really Know?International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. 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

27 authors at 7 institutions in 1 country.

Samane AbbasyDepartment of Biology, Faculty of Science, University of Guilan, Rasht, Iran; Sarem Cell Research Center, Sarem Women's Hospital, Tehran, Iran.
Fazlollah ShahrakiDepartment of Mind- Brain-Education, Institute for Cognitive Science Studies, Tehran, Iran.
Arvin HaghighatfardDepartment of Biology, North Tehran Branch, Islamic Azad University, Tehran, Iran; Department of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran. Electronic address: a.haghighatfard@iautnb.ac.ir.
Masoume Ghasemzadeh QazviniDepartment of Biology, Faculty of Science, University of Guilan, Rasht, Iran.
Sahel Towfigh RafieiDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Elnaz NoshadiradDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Mahdi FarhadiDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Horie Rezvani AslEmam Reza Hospital, Social Security Organization, Qom, Iran.
Atena Alsadat ShiryazdiDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Rana GhamariDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Zeinab TabriziDepartment of Medical Genetics, National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran.
Rashed MehrfardDepartment of Microbiology, Damghan Branch, Islamic Azad University, Damghan, Iran.
Fereshteh Esmaili KakroudiDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Mahsima AzarnooshDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Faeghe YounesiDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Narges ParsamehrDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Nooriyeh GaraeiDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Soroush AbyariDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Maede SalehiDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Maryam GholamiDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Pardis ZolfaghariDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Seyede Mahsa BagheriDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Melika PourmehrabiDepartment of Genetic, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Elham RastegarimogaddamDepartment of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran.
Elnaz NobakhtDepartment of Microbiology, Damghan Branch, Islamic Azad University, Damghan, Iran.
Elmira NobakhtDepartment of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran.
Rayan PartoviDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Islamic Azad University Medical Branch of Tehran · IRIslamic Azad University, Science and Research Branch · IRIslamic Azad University, Damghan Branch · IRUniversity of Guilan · IREmam Reza Hospital · IRInstitute for Cognitive Science Studies · IRNational Institute of Genetic Engineering and Biotechnology · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutism spectrum disorder (ASD) is a pediatric heterogeneous psychiatric and neurodevelopmental disorder with social and communication deficits, language impairment and ritualistic or repetitive behaviors. ASD has significant genetic bases but candidate genes and molecular mechanisms of disorder are not clarified. Neuregulin1 (NRG1) gene, located in 8p12 is involved in development of central nervous system and was indicated as candidate gene in schizophrenia.

methodsmRNA level of types I, II and III of NRG1 gene were studied in peripheral blood of 1540 ASD patients (IQ > 70) and 1490 control children by quantitative Real Time PCR. Also three domains of executive functions (working memory, response inhibition and vigilance) were examined in all subjects.

findingsAll three types were significantly down regulated in ASD patients. Significant deficiencies in executive functions (EF) were found in ASD patients. EF deficiencies mostly were associated with down expression of mRNA level of types I and III. Also correlations were found between NRG1 expression with gender and severity of ASD symptoms. INTERPRETATIONS: Findings primarily have been suggested involvement of NRG1 in etiology of ASD. Also correlation of NRG1 mRNA level with EF deficiencies could shed lights on EF mechanisms and may suggest targeted treatments to improve particular executive functions. FUND: Young researchers and elites club funded the project due to the annual grant of special talents of Club that gave to Arvin Haghighatfard.

Indexed as

Gene Expression RegulationAutism Spectrum DisorderChildFemaleHumansMaleNeuregulin-1Real-Time Polymerase Chain ReactionRNA, MessengerNeuregulin-1NRG1 protein, humanRNA, MessengerAutism spectrum disorderExecutive functionsGene expressionNRG1

Identifiers

PMID30415889
PMCPMC6284419
OpenAlexW2899911873

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.