Evidence map›Paper›PMID 39769462›Full record

ArticleInternational journal of molecular sciences2024

Genetic Variant Analyses Identify Novel Candidate Autism Risk Genes from a Highly Consanguineous Cohort of 104 Families from Oman.

Vijay Gupta, Afif Ben-Mahmoud, Ahmed B Idris, Jouke-Jan Hottenga, Wesal Habbab, Abeer Alsayegh, Hyung-Goo Kim, Watfa Al-Mamari, Lawrence W Stanton

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Clinical Phenotypes Associated withSultan Qaboos University medical journal · 2026
    Article
  5. Article
  6. Review
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

9 authors.

Vijay GuptaNeurological Disorder Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation, Doha P.O. Box 5825, Qatar.ORCID 0000-0002-3613-6378
Afif Ben-MahmoudNeurological Disorder Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation, Doha P.O. Box 5825, Qatar.
Ahmed B IdrisDevelopmental Paediatric Unit, Sultan Qaboos University Hospital, Sultan Qaboos University, Muscat 123, Oman.ORCID 0000-0002-5218-6711
Jouke-Jan HottengaNeurological Disorder Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation, Doha P.O. Box 5825, Qatar.ORCID 0000-0002-5668-2368
Wesal HabbabNeurological Disorder Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation, Doha P.O. Box 5825, Qatar.ORCID 0000-0001-9070-3444
Abeer AlsayeghGenomics Department, Sultan Qaboos Comprehensive Cancer Care and Research Center, University Medical City, Muscat 123, Oman.
Hyung-Goo KimNeurological Disorder Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation, Doha P.O. Box 5825, Qatar.
Watfa Al-MamariDevelopmental Paediatric Unit, Sultan Qaboos University Hospital, Sultan Qaboos University, Muscat 123, Oman.ORCID 0000-0001-7443-685X
Lawrence W StantonNeurological Disorder Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation, Doha P.O. Box 5825, Qatar.ORCID 0000-0002-3392-2779

Funding

Qatar Foundation QB06
6 · The paper itself

Abstract

Deficits in social communication, restricted interests, and repetitive behaviours are hallmarks of autism spectrum disorder (ASD). Despite high genetic heritability, the majority of clinically diagnosed ASD cases have unknown genetic origins. We performed genome sequencing on mothers, fathers, and affected individuals from 104 families with ASD in Oman, a Middle Eastern country underrepresented in international genetic studies. This approach identified 48 novel candidate genes significantly associated with ASD in Oman. In particular, 35 of these genes have been previously implicated in neurodevelopmental disorders (NDDs) in other populations, underscoring the conserved genetic basis of ASD across ethnicities. Genetic variants within these candidate genes that would impact the encoded protein included 1 insertion, 4 frameshift, 6 splicing, 12 nonsense, and 67 missense changes. Notably, 61% of the SNVs were homozygous, suggesting a prominent recessive genetic architecture for ASD in this unique population. The scarcity of genetic studies on ASD in the Arabian Peninsula has impeded the understanding of the unique genetic landscape of ASD in this region. These findings help bridge this knowledge gap and provide valuable insights into the complex genetic basis of ASD in Oman.

Indexed as

Autism Spectrum DisorderConsanguinityGenetic Predisposition to DiseaseAdultChildChild, PreschoolCohort StudiesFemaleGenetic VariationHumansMaleOmanPedigreeautism spectrum disorder (ASD)candidate ASD risk genesgenome sequencing (GS)variant of unknown significance (VUS)

Identifiers

PMID39769462
PMCPMC11679916

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.