Evidence map›Paper›PMID 23456597›Full record

SynthesisNeuromolecular medicine2013

Exploring the multifactorial nature of autism through computational systems biology: calcium and the Rho GTPase RAC1 under the spotlight.

Fares Zeidán-Chuliá, José Luiz Rybarczyk-Filho, Alla B Salmina, Ben-Hur Neves de Oliveira, Mami Noda, José Cláudio F Moreira

Abstract readSystematic Review
PubMed Publisher
In one paragraph

Synthesis in Neuromolecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Pathology and Astrocytes in Autism.Neuropsychiatric disease and treatment · 2023
    Review
  7. Article
  8. Autism Spectrum Disorder/Intellectual Disability-Associated Mutations in Trio Disrupt Neuroligin 1-Mediated Synaptogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
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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 6 institutions in 4 countries.

Fares Zeidán-ChuliáCenter of Oxidative Stress Research, Department of Biochemistry, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil. fzchulia.biomed@gmail.com
José Luiz Rybarczyk-Filho
Alla B Salmina
Ben-Hur Neves de Oliveira
Mami Noda
José Cláudio F Moreira
Krasnoyarsk State Medical University · RUKyushu University · JPUniversidade Estadual Paulista (Unesp) · BRUniversidade Federal do Rio Grande · BRUniversidade Federal do Rio Grande do Sul · BRUniversity of Rio Grande and Rio Grande Community College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism is a neurodevelopmental disorder characterized by impaired social interaction and communication accompanied with repetitive behavioral patterns and unusual stereotyped interests. Autism is considered a highly heterogeneous disorder with diverse putative causes and associated factors giving rise to variable ranges of symptomatology. Incidence seems to be increasing with time, while the underlying pathophysiological mechanisms remain virtually uncharacterized (or unknown). By systematic review of the literature and a systems biology approach, our aims were to examine the multifactorial nature of autism with its broad range of severity, to ascertain the predominant biological processes, cellular components, and molecular functions integral to the disorder, and finally, to elucidate the most central contributions (genetic and/or environmental) in silico. With this goal, we developed an integrative network model for gene-environment interactions (GENVI model) where calcium (Ca(2+)) was shown to be its most relevant node. Moreover, considering the present data from our systems biology approach together with the results from the differential gene expression analysis of cerebellar samples from autistic patients, we believe that RAC1, in particular, and the RHO family of GTPases, in general, could play a critical role in the neuropathological events associated with autism.

Indexed as

Gene-Environment InteractionGene Regulatory NetworksSystems BiologyAutistic DisorderBiopsyCalciumCell CommunicationCentral Nervous SystemCerebellumDatabases, FactualGene Expression Regulation, DevelopmentalHumansMicroarray AnalysisModels, GeneticModels, NeurologicalNerve Tissue ProteinsCalciumNerve Tissue ProteinsNeurotransmitter Agentsrac1 GTP-Binding ProteinRAC1 protein, humanrho GTP-Binding Proteins

Identifiers

PMID23456597
OpenAlexW2043484704

What Socratic 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 Socratic graph.