Identifying mechanisms underlying the intergenerational transmission of risk for attention-deficit/hyperactivity disorder (ADHD) traits can inform interventions and provide insights into the role of parents in shaping their children's outcomes. We investigated whether genetic transmission and genetic nurture (environmentally mediated effects) underlie associations between polygenic scores indexing parental risk and protective factors and their offspring's ADHD traits. This birth cohort study included 19,506 genotyped mother-father-offspring trios from the Norwegian Mother, Father and Child Cohort Study. Polygenic scores were calculated for parental factors previously associated with ADHD, including psychopathology, substance use, neuroticism, educational attainment, and cognitive performance. Mothers reported on their 8-year-old children's ADHD traits (n = 9,454 children) using the Parent/Teacher Rating Scale for Disruptive Behaviour Disorders. We found that associations between ADHD maternal and paternal polygenic scores and child ADHD traits decreased significantly when adjusting for the child polygenic score (p = 9.95 × 10 for maternal and p = 1.48 × 10 for paternal estimates), suggesting genetic transmission of ADHD risk. Similar patterns suggesting genetic transmission of risk were observed for smoking, educational attainment, and cognition. The maternal polygenic score for neuroticism remained associated with children's ADHD ratings even after adjusting for the child polygenic score, indicating genetic nurture. There was no robust evidence of genetic nurture for other parental factors. Our findings indicate that the intergenerational transmission of risk for ADHD traits is largely explained by the transmission of genetic variants from parents to offspring rather than by genetic nurture. Observational associations between parental factors and childhood ADHD outcomes should not be interpreted as evidence for predominantly environmentally mediated effects.
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http://dx.doi.org/10.1038/s41380-022-01863-6 | DOI Listing |
Br J Psychiatry
January 2025
Department of Psychology, Nottingham Trent University, UK; and Institute of Human Sciences, University of Oxford, UK.
Background: Reliable and specific biomarkers that can distinguish autism spectrum disorders (ASDs) from commonly co-occurring attention-deficit/hyperactivity disorder (ADHD) are lacking, causing misses and delays in diagnosis, and reducing access to interventions and quality of life.
Aims: To examine whether an innovative, brief (1-min), videogame method called Computerised Assessment of Motor Imitation (CAMI), can identify ASD-specific imitation differences compared with neurotypical children and children with ADHD.
Method: This cross-sectional study used CAMI alongside standardised parent-report (Social Responsiveness Scale, Second Edition) and observational measures of autism (Autism Diagnostic Observation Schedule-Second Edition; ADOS-2), ADHD (Conners) and motor ability (Physical and Neurological Examination for Soft Signs).
Prog Neuropsychopharmacol Biol Psychiatry
January 2025
Laboratory of Molecular Neurobiology and Behavior, Department of Neurobiology, Institute for Biological Research "Siniša Stanković" - National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia. Electronic address:
Attention-Deficit/Hyperactivity Disorder (ADHD) is associated with an increased risk of Parkinson's disease (PD) and other synucleinopathies later in life. The severity of the ADHD phenotype may play a significant role in this association. There is no indication that any of the existing animal models can unify these disorders.
View Article and Find Full Text PDFEur Eat Disord Rev
January 2025
Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK.
Objective: This review maps existing literature on the prevalence of autism and ADHD in adult patients with Bulimia Nervosa (BN) and Binge Eating Disorder (BED); patient and stakeholder perspectives on this comorbidity; clinical differences in this population; and potential treatment adaptations or adjunct therapies. This is with the aim to inform future research priorities to improve clinical practice.
Method: As pre-registered, and following PRISMA guidelines, six databases (Embase, MEDLINE via Ovid, PsycINFO, Web of Science, CENTRAL, and Scopus) were searched for studies regarding autism and/or ADHD (diagnosed, probable, or traits) in adult patients with BN or BED.
Res Involv Engagem
January 2025
Department of Experimental Psychology, University of Oxford, Oxford, UK.
Programmes designed to support children with known, or increased likelihood of, autism or ADHD often focus on reducing behaviours central to a clinical diagnosis. However, supporting children to pursue their own goals and cope with everyday life through fostering executive function (EF) development, without enforcing neuro-normative assumptions, may be more acceptable to neurodivergent people, and more beneficial. The co-production process for this neurodiversity-affirming programme involved: Review of research priorities identified during published public-and-clinician consultations; iterative programme development through two pilot rounds with a general community sample; and consultation with stakeholders (parents with a connection to autism or ADHD, alongside early years specialists, psychologists and therapists) to check acceptability of the proposal, and refine the logic model and materials.
View Article and Find Full Text PDFObjectives: Non-adherence to medication is common in the adult ADHD clinical group. The goal of this pre-registered study was to examine whether the DSM-5 Alternative Model of Personality Disorder (AMPD), generality personality dysfunction (LPFS-BF 2.0) or maladaptive personality traits (PID-5), can predict time to premature discontinuation of pharmacological treatment beyond other known factors.
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