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2 results

  • 9.2 - Attention Deficit Hyperactivity Disorder

  • from 9 - Integrated Neurobiology of Specific Syndromes and Treatments
  • Edited by Mary-Ellen Lynall, University of Cambridge, Peter B. Jones, University of Cambridge, Stephen M. Stahl, University of California, San Diego
  • Book:
    Cambridge Textbook of Neuroscience for Psychiatrists
    Published online:
    08 November 2023
    Print publication:
    16 November 2023, pp 397-402

  • Summary

    Attention deficit hyperactivity disorder (ADHD) is a childhood-onset disorder with a prevalence of 5%. It is clinically defined by symptoms of inattention, motor hyperactivity and impulsivity. In addition to the core symptoms, it has also been associated with impairment in cognitive domains. ADHD is highly heritable and multifactorial in origin; multiple genes and non-inherited factors contribute to the aetiology of the disorder. ADHD has been associated with slower maturation of long white matter tracts and decreased volume in brain regions relevant for executive function, sustained attention, impulse suppression and regulation of motor activity. In addition to structural brain changes, a range of brain networks and dysregulation of neurotransmitter signalling have also been associated with ADHD. However, no diagnostic neurobiological markers are currently available for clinical use.

  • Polygenic association between attention-deficit/hyperactivity disorder liability and cognitive impairments

  • Isabella Vainieri, Joanna Martin, Anna-Sophie Rommel, Philip Asherson, Tobias Banaschewski, Jan Buitelaar, Bru Cormand, Jennifer Crosbie, Stephen V. Faraone, Barbara Franke, Sandra K. Loo, Ana Miranda, Iris Manor, Robert D. Oades, Kirstin L. Purves, J. Antoni Ramos-Quiroga, Marta Ribasés, Herbert Roeyers, Aribert Rothenberger, Russell Schachar, Joseph Sergeant, Hans-Christoph Steinhausen, Pieter J. Vuijk, Alysa E. Doyle, Jonna Kuntsi
  • Journal:
    Psychological Medicine / Volume 52 / Issue 14 / October 2022
    Published online by Cambridge University Press:
    03 February 2021, pp. 3150-3158
    • Article
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  • Background

    A recent genome-wide association study (GWAS) identified 12 independent loci significantly associated with attention-deficit/hyperactivity disorder (ADHD). Polygenic risk scores (PRS), derived from the GWAS, can be used to assess genetic overlap between ADHD and other traits. Using ADHD samples from several international sites, we derived PRS for ADHD from the recent GWAS to test whether genetic variants that contribute to ADHD also influence two cognitive functions that show strong association with ADHD: attention regulation and response inhibition, captured by reaction time variability (RTV) and commission errors (CE).

    Methods

    The discovery GWAS included 19 099 ADHD cases and 34 194 control participants. The combined target sample included 845 people with ADHD (age: 8–40 years). RTV and CE were available from reaction time and response inhibition tasks. ADHD PRS were calculated from the GWAS using a leave-one-study-out approach. Regression analyses were run to investigate whether ADHD PRS were associated with CE and RTV. Results across sites were combined via random effect meta-analyses.

    Results

    When combining the studies in meta-analyses, results were significant for RTV (R2 = 0.011, β = 0.088, p = 0.02) but not for CE (R2 = 0.011, β = 0.013, p = 0.732). No significant association was found between ADHD PRS and RTV or CE in any sample individually (p > 0.10).

    Conclusions

    We detected a significant association between PRS for ADHD and RTV (but not CE) in individuals with ADHD, suggesting that common genetic risk variants for ADHD influence attention regulation.