Evidence map›Paper›PMID 30705255›Full record

ArticleTranslational psychiatry2019

Disruption of mTOR and MAPK pathways correlates with severity in idiopathic autism.

Eleonora Rosina, Barbara Battan, Martina Siracusano, Lorena Di Criscio, Fiona Hollis, Laura Pacini, Paolo Curatolo, Claudia Bagni

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 4 pooled it
10.3field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 4 syntheses or guidelines pooled it, 140 citations in OpenAlex.

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10 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 2 countries.

Eleonora RosinaDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Barbara BattanDepartment of Systems Medicine, Division of Child Neurology and Psychiatry, University Hospital of Tor Vergata, Rome, Italy.
Martina SiracusanoDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Lorena Di CriscioDepartment of Systems Medicine, Division of Child Neurology and Psychiatry, University Hospital of Tor Vergata, Rome, Italy.
Fiona HollisDepartment of Fundamental Neurosciences, University of Lausanne, Lausanne, Switzerland.
Laura PaciniDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Paolo CuratoloDepartment of Systems Medicine, Division of Child Neurology and Psychiatry, University Hospital of Tor Vergata, Rome, Italy.
Claudia BagniDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy. claudia.bagni@unil.ch.
University of Rome Tor Vergata · ITUniversity of Lausanne · CHUniversity of L'Aquila · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular signature underlying autism spectrum disorder remains largely unknown. This study identifies differential expression of mTOR and MAPK pathways in patients affected by mild and severe idiopathic autism. A total of 55 subjects were enrolled, of which 22 were typically developing individuals and 33 were patients aged between 3 and 11 years, with autism spectrum disorder. A detailed history, including physical examination, developmental evaluation, mental health history and autism diagnostic observation schedule were performed for each patient. Components of the mTOR and MAPK signalling pathways were analysed from peripheral blood at the protein level. Patients were then stratified according to their clinical phenotypes, and the molecular profiling was analysed in relation to the degree of autism severity. In this cohort of patients, we identified increased activity of mTOR and the MAPK pathways, key regulators of synaptogenesis and protein synthesis. Specifically, rpS6, p-eIF4E, TSC1 and p-MNK1 expression discriminated patients according to their clinical diagnosis, suggesting that components of protein synthesis signalling pathways might constitute a molecular signature of clinical severity in autism spectrum disorder.

Indexed as

Autism Spectrum DisorderChildChild, PreschoolFemaleHumansIntracellular Signaling Peptides and ProteinsMaleMAP Kinase Signaling SystemNeurogenesisNucleocytoplasmic Transport ProteinsProtein Serine-Threonine KinasesRibosomal Protein S6 Kinases, 90-kDaTOR Serine-Threonine KinasesTuberous Sclerosis Complex 1 ProteinEIF4ENIF1 protein, humanIntracellular Signaling Peptides and ProteinsMKNK1 protein, humanMTOR protein, humanNucleocytoplasmic Transport ProteinsProtein Serine-Threonine KinasesRibosomal Protein S6 Kinases, 90-kDaRPS6KA1 protein, humanTOR Serine-Threonine KinasesTSC1 protein, humanTuberous Sclerosis Complex 1 Protein

Identifiers

PMID30705255
PMCPMC6355879
OpenAlexW2912420851

What OpenQuestion holds

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LicenceCC BY
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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.