Evidence map›Paper›PMID 33608048›Full record

Trial reportMolecular autism2021

Modulation of atypical brain activation during executive functioning in autism: a pharmacological MRI study of tianeptine.

Robert H Wichers, James L Findon, Auke Jelsma, Vincent Giampietro, Vladimira Stoencheva, Dene M Robertson, Clodagh M Murphy, Sarah Blainey, Grainne McAlonan, Christine Ecker and 3 more

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Molecular autism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. 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

13 authors at 3 institutions in 3 countries.

Robert H WichersDepartment of Forensic and Neurodevelopmental Sciences, The Sackler Centre for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, PO50 De Crespigny Park, Denmark Hill, London, SE5 8AF, UK. rob.wichers@kcl.ac.uk.
James L FindonDepartment of Forensic and Neurodevelopmental Sciences, The Sackler Centre for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, PO50 De Crespigny Park, Denmark Hill, London, SE5 8AF, UK.
Auke JelsmaDepartment of Forensic and Neurodevelopmental Sciences, The Sackler Centre for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, PO50 De Crespigny Park, Denmark Hill, London, SE5 8AF, UK.
Vincent GiampietroDepartment of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Vladimira StoenchevaBehavioural and Developmental Psychiatry Clinical Academic Group, South London and Maudsley NHS Trust, London, UK.
Dene M RobertsonDepartment of Forensic and Neurodevelopmental Sciences, The Sackler Centre for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, PO50 De Crespigny Park, Denmark Hill, London, SE5 8AF, UK.
Clodagh M MurphyDepartment of Forensic and Neurodevelopmental Sciences, The Sackler Centre for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, PO50 De Crespigny Park, Denmark Hill, London, SE5 8AF, UK.
Sarah BlaineyDepartment of Forensic and Neurodevelopmental Sciences, The Sackler Centre for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, PO50 De Crespigny Park, Denmark Hill, London, SE5 8AF, UK.
Grainne McAlonanDepartment of Forensic and Neurodevelopmental Sciences, The Sackler Centre for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, PO50 De Crespigny Park, Denmark Hill, London, SE5 8AF, UK.
Christine EckerDepartment of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt am Main, Goethe-University, Frankfurt am Main, Germany.
Katya RubiaDepartment of Child and Adolescent Psychiatry, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Declan G M MurphyDepartment of Forensic and Neurodevelopmental Sciences, The Sackler Centre for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, PO50 De Crespigny Park, Denmark Hill, London, SE5 8AF, UK.
Eileen M DalyDepartment of Forensic and Neurodevelopmental Sciences, The Sackler Centre for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, PO50 De Crespigny Park, Denmark Hill, London, SE5 8AF, UK.
King's College London · GBSouth London and Maudsley NHS Foundation Trust · GBGoethe University Frankfurt · DE

Funding

Department of HealthMedical Research Council MR/N026063/1
6 · The paper itself

Abstract

backgroundAutism spectrum disorder (ASD) is associated with deficits in executive functioning (EF), and these have been suggested to contribute to core as well as co-occurring psychiatric symptoms. The biological basis of these deficits is unknown but may include the serotonergic system, which is involved both in regulating EF in neurotypical populations and in the pathophysiology of ASD. We previously demonstrated that reducing serotonin by acute tryptophan depletion (ATD) shifts differences in brain function during performance of EF tasks towards control levels. However, ATD cannot be easily used in the clinic, and we therefore need to adopt alternative approaches to challenge the serotonin system. Hence, we investigated the role of the serotonergic modulator tianeptine on EF networks in ASD.

methodWe conducted a pharmacological magnetic resonance imaging study, using a randomized double-blind crossover design, to compare the effect of an acute dosage of 12.5 mg tianeptine and placebo on brain activation during two EF tasks (of response inhibition and sustained attention) in 38 adult males: 19 with ASD and 19 matched controls.

resultsUnder placebo, compared to controls, individuals with ASD had atypical brain activation in response inhibition regions including the inferior frontal cortex, premotor regions and cerebellum. During sustained attention, individuals with ASD had decreased brain activation in the right middle temporal cortex, right cuneus and left precuneus. Most of the case-control differences in brain function observed under placebo conditions were abolished by tianeptine administration. Also, within ASD individuals, brain functional differences were shifted significantly towards control levels during response inhibition in the inferior frontal and premotor cortices. LIMITATIONS: We conducted a pilot study using a single dose of tianeptine, and therefore, we cannot comment on long-term outcome.

conclusionsOur findings provide the first evidence that tianeptine can shift atypical brain activation during EF in adults with ASD towards control levels. Future studies should investigate whether this shift in the biology of ASD is maintained after prolonged treatment with tianeptine and whether it improves clinical symptoms.

Indexed as

AdultAntidepressive Agents, TricyclicAttentionAutistic DisorderBrainCross-Over StudiesDouble-Blind MethodExecutive FunctionHumansMagnetic Resonance ImagingMaleMiddle AgedPilot ProjectsThiazepinesYoung AdultAntidepressive Agents, TricyclicThiazepinestianeptineAutism spectrum disorderExecutive functioningfMRISerotoninTianeptine

Identifiers

PMID33608048
PMCPMC7893772
OpenAlexW3123709594

What OpenQuestion holds

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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.