ArticlePsychoneuroendocrinology2012
Steroid sulfatase-deficient mice exhibit endophenotypes relevant to attention deficit hyperactivity disorder.
Article in Psychoneuroendocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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.
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.
Who cites it
24 citing papers in PubMed, 49 citations in OpenAlex.
- Physiological and Behavioural Characterisation of a Novel Steroid Sulfatase-Deficient Mouse.Genes, brain, and behavior · 2026Article
- An updated review on animal models to study attention-deficit hyperactivity disorder.Translational psychiatry · 2024Review
- Maternal Xp22.31 copy-number variations detected in non-invasive prenatal screening effectively guide the prenatal diagnosis of X-linked ichthyosis.Frontiers in genetics · 2022Article
- A new molecular risk pathway for postpartum mood disorders: clues from steroid sulfatase-deficient individuals.Archives of women's mental health · 2021Review
- Medical and neurobehavioural phenotypes in carriers of X-linked ichthyosis-associated genetic deletions in the UK Biobank.Journal of medical genetics · 2020Article
- Behavioural and psychiatric phenotypes in female carriers of genetic mutations associated with X-linked ichthyosis.PloS one · 2019Article
- Brain Gene Expression in a Novel Mouse Model of Postpartum Mood Disorder.Translational neuroscience · 2019Article
- X-Chromosome Effects on Attention Networks: Insights from Imaging Resting-State Networks in Turner Syndrome.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Exploring the Validity of Proposed Transgenic Animal Models of Attention-Deficit Hyperactivity Disorder (ADHD).Molecular neurobiology · 2018Review
- X-linked ichthyosis associated with psychosis and behavioral abnormalities: a case report.Journal of medical case reports · 2017Article
- Understanding the pathophysiology of postpartum psychosis: Challenges and new approaches.World journal of psychiatry · 2017Review
- Polymorphisms of STS gene and SULT2A1 gene and neurosteroid levels in Han Chinese boys with attention-deficit/hyperactivity disorder: an exploratory investigation.Scientific reports · 2017Article
- Attention deficit hyperactivity disorder (ADHD) in phenotypically similar neurogenetic conditions: Turner syndrome and the RASopathies.Journal of neurodevelopmental disorders · 2017Review
- Behavioural and Psychiatric Phenotypes in Men and Boys with X-Linked Ichthyosis: Evidence from a Worldwide Online Survey.PloS one · 2016Article
- Genetic and pharmacological modulation of the steroid sulfatase axis improves response control; comparison with drugs used in ADHD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
- Mouse model systems to study sex chromosome genes and behavior: relevance to humans.Frontiers in neuroendocrinology · 2014Review
- Altered brain gene expression but not steroid biochemistry in a genetic mouse model of neurodevelopmental disorder.Molecular autism · 2014Article
- Role of cholesterol sulfate in epidermal structure and function: lessons from X-linked ichthyosis.Biochimica et biophysica acta · 2014Review
- Transgenic mouse models for ADHD.Cell and tissue research · 2013Review
- Biological mechanisms associated with increased perseveration and hyperactivity in a genetic mouse model of neurodevelopmental disorder.Psychoneuroendocrinology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Attention Deficit Hyperactivity Disorder (ADHD) is a common neurodevelopmental condition characterised by inattention, impulsivity and hyperactivity; it is frequently co-morbid with anxiety and conduct disorders, sleep perturbation and abnormal consummatory behaviours. Recent studies have implicated the neurosteroid-modulating enzyme steroid sulfatase (STS) as a modulator of ADHD-related endophenotypes. The effects of steroid sulfatase deficiency on homecage activity, feeding/drinking behaviours, anxiety-related behaviours (assayed in light-dark box and open field paradigms), social dominance and serum steroid hormone levels were determined by comparing 40,XY and 39,X(Y*)O mice. Subsequently, mice administered the steroid sulfatase inhibitor COUMATE acutely were compared to vehicle-treated mice on behavioural tasks sensitive to enzyme deficiency to dissociate between its developmental and ongoing effects. 39,X(Y*)O mice exhibited heightened reactivity to a novel environment, hyperactivity in the active phase, and increased water (but not food) consumption relative to 40,XY mice during a 24h period; the former group also demonstrated evidence for heightened emotional reactivity. There was no difference in social dominance between the 40,XY and 39,X(Y*)O mice. COUMATE administration had no effect on homecage activity, water consumption or anxiety measures in the open field. 39,X(Y*)O mice exhibited significantly lower dehydroepiandrosterone (DHEA) serum levels than 40,XY mice, but equivalent corticosterone levels. Together with previous data, the present results suggest that steroid sulfatase may influence core and associated ADHD behavioural endophenotypes via both developmental and ongoing mechanisms, and that the 39,X(Y*)O model may represent a useful tool for elucidating the neurobiological basis of these endophenotypes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.