Evidence map›Paper›PMID 33523602›Full record

ArticleBrain and behavior2021

REVERSE phenotyping-Can the phenotype following constitutive Tph2 gene inactivation in mice be transferred to children and adolescents with and without adhd?

Atae Akhrif, Arunima Roy, Katharina Peters, Klaus-Peter Lesch, Marcel Romanos, Angelika Schmitt-Böhrer, Susanne Neufang

Open access · goldAbstract read
In one paragraph

Article in Brain and behavior, 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
0.5field-weighted citation impact, top 40% 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, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Attention-deficit/hyperactive disorder updates.Frontiers in molecular neuroscience · 2022
    Review
  5. Article
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

7 authors at 4 institutions in 4 countries.

Atae AkhrifDepartment of Child and Adolescent Psychiatry, Center of Mental Health, University of Würzburg, Würzburg, Germany.
Arunima RoyThe Royal's Institute of Mental Health Research, University of Ottawa, Ottawa, Canada.
Katharina PetersDepartment of Child and Adolescent Psychiatry, Center of Mental Health, University of Würzburg, Würzburg, Germany.
Klaus-Peter LeschDivision of Molecular Psychiatry, Center of Mental Health, University of Würzburg, Würzburg, Germany.
Marcel RomanosDepartment of Child and Adolescent Psychiatry, Center of Mental Health, University of Würzburg, Würzburg, Germany.
Angelika Schmitt-BöhrerDepartment of Psychiatry, Psychosomatics and Psychotherapy, Center of Mental Health, University of Würzburg, Würzburg, Germany.
Susanne NeufangComparative Psychology, Institute of Experimental Psychology, Heinrich-Heine University of Düsseldorf, Düsseldorf, Germany.ORCID 0000-0002-4927-2969
University of Würzburg · DEHeinrich Heine University Düsseldorf · DESechenov University · RUUniversity of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionExperimental models of neuropsychiatric disorders, for example, ADHD, are used to mimic specific phenotypic traits of a complex human disorder. However, it remains unresolved to what extent the animal phenotype reflects the specific human trait. The null mutant mouse of the serotonin-synthesizing tryptophan hydroxylase-2 (Tph2

methods58 participants (6 females, 8-18 years) were examined, of whom 32 were diagnosed with ADHD. All participants were phenotyped for impulsivity, aggression, and anxiety using questionnaires, behavioral tests, and MRI scanning while performing the 4-choice serial reaction time task. Additionally, participants were genotyped for the TPH2 G-703T (rs4570625) polymorphism. To analyze the relation between TPH2 G-703T variants and the impulsive/aggressive/anxious phenotype, mediation analyses were performed using behavioral and MRI data as potential mediators.

resultsWe found that the relation between TPH2 G-703T and aggression as part of the reverse Tph2

conclusionAt the example of trait aggression, our results support the assumption that the Tph2 null mutant mouse reflects the TPH2 G-703T-dependent phenotype in humans. Additionally, we conclude that "reverse phenotyping" is a promising method to validate experimental models and human findings for refined analysis of disease mechanisms.

Indexed as

Attention Deficit Disorder with HyperactivityAnimalsGene SilencingGenotypeMicePhenotypeTryptophan HydroxylaseTph2 protein, mouseTryptophan Hydroxylaseaggressionanxietyattention-deficit/hyperactivity disorder (ADHD)impulsivityTPH2 G-703T (rs4570625) polymorphismTph2-/- mousetryptophan hydroxylase-2 (TPH2)

Identifiers

PMID33523602
PMCPMC8119824
OpenAlexW3127317334

What OpenQuestion holds

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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.