Evidence map›Paper›PMID 25386956›Full record

ArticleTranslational psychiatry2014

The serotonin-N-acetylserotonin-melatonin pathway as a biomarker for autism spectrum disorders.

C Pagan, R Delorme, J Callebert, H Goubran-Botros, F Amsellem, X Drouot, C Boudebesse, K Le Dudal, N Ngo-Nguyen, H Laouamri and 4 more

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

Article in Translational psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 3 pooled it
6.7field-weighted citation impact, top 2% 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

84 citing papers in PubMed, 3 syntheses or guidelines pooled it, 170 citations in OpenAlex.

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24 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

14 authors at 6 institutions in 2 countries.

C Pagan1] Service de Biochimie et Biologie Moléculaire, Department of Biochemistry, University Hospital Lariboisière, AP-HP, INSERM U942, Paris, France [2] University Paris Descartes, Sorbonne Paris Cité, Paris, France [3] Human Genetics and Cognitive Functions, CNRS URA 2182 « Genes, Synapses and Cognition », Institut Pasteur, Paris, France [4] Fondation FondaMental, Créteil, France.
R Delorme1] Human Genetics and Cognitive Functions, CNRS URA 2182 « Genes, Synapses and Cognition », Institut Pasteur, Paris, France [2] Fondation FondaMental, Créteil, France [3] Department of Child and Adolescent Psychiatry, Robert-Debré Hospital, AP-HP, Paris, France [4] University Paris Diderot, Sorbonne Paris Cité, Paris, France.
J Callebert1] Service de Biochimie et Biologie Moléculaire, Department of Biochemistry, University Hospital Lariboisière, AP-HP, INSERM U942, Paris, France [2] University Paris Descartes, Sorbonne Paris Cité, Paris, France.
H Goubran-BotrosHuman Genetics and Cognitive Functions, CNRS URA 2182 « Genes, Synapses and Cognition », Institut Pasteur, Paris, France.
F Amsellem1] Fondation FondaMental, Créteil, France [2] Department of Child and Adolescent Psychiatry, Robert-Debré Hospital, AP-HP, Paris, France.
X Drouot1] Fondation FondaMental, Créteil, France [2] INSERM U955, Psychiatry Genetic, Créteil, France.
C Boudebesse1] Fondation FondaMental, Créteil, France [2] INSERM U955, Psychiatry Genetic, Créteil, France [3] Department of Psychiatry, University Hospital Henri Mondor, AP-HP, University Paris-Est Créteil, Créteil, France.
K Le Dudal1] Fondation FondaMental, Créteil, France [2] INSERM, CIC 1430 and Biological Resource Platform, Henri Mondor Hospital, AP-HP, Créteil, France.
N Ngo-NguyenFondation FondaMental, Créteil, France.
H LaouamriFondation FondaMental, Créteil, France.
C Gillberg1] Gillberg Neuropsychiatry Centre, University of Gothenburg, Goteborg, Sweden [2] Institute of Child Health, University College London, London, UK.
M Leboyer1] Fondation FondaMental, Créteil, France [2] INSERM U955, Psychiatry Genetic, Créteil, France [3] Department of Psychiatry, University Hospital Henri Mondor, AP-HP, University Paris-Est Créteil, Créteil, France.
T Bourgeron1] Human Genetics and Cognitive Functions, CNRS URA 2182 « Genes, Synapses and Cognition », Institut Pasteur, Paris, France [2] Fondation FondaMental, Créteil, France [3] University Paris Diderot, Sorbonne Paris Cité, Paris, France.
J-M Launay1] Service de Biochimie et Biologie Moléculaire, Department of Biochemistry, University Hospital Lariboisière, AP-HP, INSERM U942, Paris, France [2] University Paris Descartes, Sorbonne Paris Cité, Paris, France [3] Fondation FondaMental, Créteil, France.
Fondation FondaMental · FRAssistance Publique – Hôpitaux de Paris · FRGènes, synapses et cognition · FRInstitut Pasteur · FRSorbonne Paris Cité · FRUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated whole-blood serotonin and decreased plasma melatonin (a circadian synchronizer hormone that derives from serotonin) have been reported independently in patients with autism spectrum disorders (ASDs). Here, we explored, in parallel, serotonin, melatonin and the intermediate N-acetylserotonin (NAS) in a large cohort of patients with ASD and their relatives. We then investigated the clinical correlates of these biochemical parameters. Whole-blood serotonin, platelet NAS and plasma melatonin were assessed in 278 patients with ASD, their 506 first-degree relatives (129 unaffected siblings, 199 mothers and 178 fathers) and 416 sex- and age-matched controls. We confirmed the previously reported hyperserotonemia in ASD (40% (35-46%) of patients), as well as the deficit in melatonin (51% (45-57%)), taking as a threshold the 95th or 5th percentile of the control group, respectively. In addition, this study reveals an increase of NAS (47% (41-54%) of patients) in platelets, pointing to a disruption of the serotonin-NAS-melatonin pathway in ASD. Biochemical impairments were also observed in the first-degree relatives of patients. A score combining impairments of serotonin, NAS and melatonin distinguished between patients and controls with a sensitivity of 80% and a specificity of 85%. In patients the melatonin deficit was only significantly associated with insomnia. Impairments of melatonin synthesis in ASD may be linked with decreased 14-3-3 proteins. Although ASDs are highly heterogeneous, disruption of the serotonin-NAS-melatonin pathway is a very frequent trait in patients and may represent a useful biomarker for a large subgroup of individuals with ASD.

Indexed as

AdolescentAdultBiomarkersChildChild Development Disorders, PervasiveFemaleHumansMaleMelatoninParentsSerotoninSiblingsSignal TransductionBiomarkersMelatoninN-acetylserotoninSerotonin

Identifiers

PMID25386956
PMCPMC4259991
OpenAlexW2073804342

What OpenQuestion holds

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LicenceCC BY-NC-SA
Read underepoch 390

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.