Evidence map›Paper›PMID 24842408›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014

Genetic and pharmacological modulation of the steroid sulfatase axis improves response control; comparison with drugs used in ADHD.

William Davies, Trevor Humby, Simon Trent, Jessica B Eddy, Obah A Ojarikre, Lawrence S Wilkinson

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Reversal Learning Performance in the XYFrontiers in behavioral neuroscience · 2019
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. A genetic variant withinBrain and behavior · 2017
    Article
  17. Article
  18. Article
  19. 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

6 authors at 2 institutions in 1 country.

William Davies1] Behavioral Genetics Group, Schools of Psychology and Medicine, Cardiff University, Cardiff, UK [2] MRC Centre for Neuropsychiatric Genetics and Genomics and Institute of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK [3] Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.
Trevor Humby1] Behavioral Genetics Group, Schools of Psychology and Medicine, Cardiff University, Cardiff, UK [2] MRC Centre for Neuropsychiatric Genetics and Genomics and Institute of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK [3] Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.
Simon Trent1] Behavioral Genetics Group, Schools of Psychology and Medicine, Cardiff University, Cardiff, UK [2] MRC Centre for Neuropsychiatric Genetics and Genomics and Institute of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK [3] Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.
Jessica B Eddy1] Behavioral Genetics Group, Schools of Psychology and Medicine, Cardiff University, Cardiff, UK [2] MRC Centre for Neuropsychiatric Genetics and Genomics and Institute of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK.
Obah A OjarikreMRC National Institute for Medical Research, London, Cardiff, UK.
Lawrence S Wilkinson1] Behavioral Genetics Group, Schools of Psychology and Medicine, Cardiff University, Cardiff, UK [2] MRC Centre for Neuropsychiatric Genetics and Genomics and Institute of Psychological Medicine and Clinical Neurosciences, School of Medicine, Cardiff University, Cardiff, UK [3] Neuroscience and Mental Health Research Institute, Cardiff University, Cardiff, UK.
Cardiff University · GBThe Francis Crick Institute · GB

Funding

Medical Research Council G0900636Medical Research Council MR/L010305/1Medical Research Council U117532009
6 · The paper itself

Abstract

Maladaptive response control is a feature of many neuropsychiatric conditions, including attention deficit hyperactivity disorder (ADHD). As ADHD is more commonly diagnosed in males than females, a pathogenic role for sex-linked genes has been suggested. Deletion or point mutation of the X-linked STS gene, encoding the enzyme steroid sulfatase (STS) influences risk for ADHD. We examined whether deletion of the Sts gene in the 39,X(Y*)O mouse model, or pharmacological manipulation of the STS axis, via administration of the enzyme substrate dehydroepiandrosterone sulfate or the enzyme inhibitor COUMATE, influenced behavior in a novel murine analog of the stop-signal reaction time task used to detect inhibitory deficits in individuals with ADHD. Unexpectedly, both the genetic and pharmacological treatments resulted in enhanced response control, manifest as highly specific effects in the ability to cancel a prepotent action. For all three manipulations, the effect size was comparable to that seen with the commonly used ADHD therapeutics methylphenidate and atomoxetine. Hence, converging genetic and pharmacological evidence indicates that the STS axis is involved in inhibitory processes and can be manipulated to give rise to improvements in response control. While the precise neurobiological mechanism(s) underlying the effects remain to be established, there is the potential for exploiting this pathway in the treatment of disorders where failures in behavioral inhibition are prominent.

Indexed as

Inhibition, PsychologicalAdrenergic Uptake InhibitorsAnimalsAtomoxetine HydrochlorideAttention Deficit Disorder with HyperactivityCentral Nervous System AgentsCentral Nervous System StimulantsCoumarinsDehydroepiandrosterone SulfateDisease Models, AnimalEnzyme InhibitorsMaleMethylphenidateMice, TransgenicNeuropsychological TestsPropylamines4-methylcoumarin 7-O-sulfamateAdrenergic Uptake InhibitorsAtomoxetine HydrochlorideCentral Nervous System AgentsCentral Nervous System StimulantsCoumarinsDehydroepiandrosterone SulfateEnzyme InhibitorsMethylphenidatePropylaminesSteryl-SulfataseSulfonamides

Identifiers

PMID24842408
PMCPMC4140762
OpenAlexW2078001247

What OpenQuestion 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 OpenQuestion graph.