Evidence map›Paper›PMID 32066720›Full record

ArticleTranslational psychiatry2020

Identification of biological mechanisms underlying a multidimensional ASD phenotype using machine learning.

Muhammad Asif, Hugo F M C Martiniano, Ana Rita Marques, João Xavier Santos, Joana Vilela, Celia Rasga, Guiomar Oliveira, Francisco M Couto, Astrid M Vicente

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 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
1.9field-weighted citation impact, top 15% 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, 29 citations in OpenAlex.

  1. Efficacy and Safety of AltibrainCurrent pharmaceutical design · 2025
    Trial
  2. Shared and distinct phenotypic profiles among neurodevelopmental disorder genes.medRxiv : the preprint server for health sciences · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Prematurity and Genetic Liability for Autism Spectrum Disorder.medRxiv : the preprint server for health sciences · 2025
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  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

9 authors at 2 institutions in 2 countries.

Muhammad AsifInstituto Nacional de Saúde Doutor Ricardo Jorge, Avenida Padre Cruz, 1649-016, Lisboa, Portugal.
Hugo F M C MartinianoInstituto Nacional de Saúde Doutor Ricardo Jorge, Avenida Padre Cruz, 1649-016, Lisboa, Portugal.
Ana Rita MarquesInstituto Nacional de Saúde Doutor Ricardo Jorge, Avenida Padre Cruz, 1649-016, Lisboa, Portugal.ORCID http://orcid.org/0000-0003-4144-7020
João Xavier SantosInstituto Nacional de Saúde Doutor Ricardo Jorge, Avenida Padre Cruz, 1649-016, Lisboa, Portugal.
Joana VilelaInstituto Nacional de Saúde Doutor Ricardo Jorge, Avenida Padre Cruz, 1649-016, Lisboa, Portugal.
Celia RasgaInstituto Nacional de Saúde Doutor Ricardo Jorge, Avenida Padre Cruz, 1649-016, Lisboa, Portugal.
Guiomar OliveiraUnidade de Neurodesenvolvimento e Autismo (UNDA), Serviço do Centro de Desenvolvimento da Criança, Centro de Investigação e Formação Clínica, Hospital Pediátrico, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal.
Francisco M CoutoFaculdade de Ciências, LASIGE, Universidade de Lisboa, Lisboa, Portugal.
Astrid M VicenteInstituto Nacional de Saúde Doutor Ricardo Jorge, Avenida Padre Cruz, 1649-016, Lisboa, Portugal. astrid.vicente@insa.min-saude.pt.ORCID http://orcid.org/0000-0001-7134-8037
University of Lisbon · PTHospitais da Universidade de Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complex genetic architecture of Autism Spectrum Disorder (ASD) and its heterogeneous phenotype makes molecular diagnosis and patient prognosis challenging tasks. To establish more precise genotype-phenotype correlations in ASD, we developed a novel machine-learning integrative approach, which seeks to delineate associations between patients' clinical profiles and disrupted biological processes, inferred from their copy number variants (CNVs) that span brain genes. Clustering analysis of the relevant clinical measures from 2446 ASD cases in the Autism Genome Project identified two distinct phenotypic subgroups. Patients in these clusters differed significantly in ADOS-defined severity, adaptive behavior profiles, intellectual ability, and verbal status, the latter contributing the most for cluster stability and cohesion. Functional enrichment analysis of brain genes disrupted by CNVs in these ASD cases identified 15 statistically significant biological processes, including cell adhesion, neural development, cognition, and polyubiquitination, in line with previous ASD findings. A Naive Bayes classifier, generated to predict the ASD phenotypic clusters from disrupted biological processes, achieved predictions with a high precision (0.82) but low recall (0.39), for a subset of patients with higher biological Information Content scores. This study shows that milder and more severe clinical presentations can have distinct underlying biological mechanisms. It further highlights how machine-learning approaches can reduce clinical heterogeneity by using multidimensional clinical measures, and establishes genotype-phenotype correlations in ASD. However, predictions are strongly dependent on patient's information content. Findings are therefore a first step toward the translation of genetic information into clinically useful applications, and emphasize the need for larger datasets with very complete clinical and biological information.

Indexed as

Autism Spectrum DisorderBayes TheoremDNA Copy Number VariationsHumansMachine LearningPhenotype

Identifiers

PMID32066720
PMCPMC7026098
OpenAlexW3003854432

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.