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The Separation of ADHD Inattention and Hyperactivity-Impulsivity Symptoms: Pathways from Genetic Effects to Cognitive Impairments and Symptoms
Open accessAbstract
Both shared and unique genetic risk factors underlie the two symptom domains of attention deficit hyperactivity disorder (ADHD): inattention and hyperactivity-impulsivity. The developmental course and relationship to co-occurring disorders differs across the two symptom domains, highlighting the importance of their partially distinct etiologies. Familial cognitive impairment factors have been identified in ADHD, but whether they show specificity in relation to the two ADHD symptom domains remains poorly understood. We aimed to investigate whether different cognitive impairments are genetically linked to the ADHD symptom domains of inattention versus hyperactivity-impulsivity. We conducted multivariate genetic model fitting analyses on ADHD symptom scores and cognitive data, from go/no-go and fast tasks, collected on a population twin sample of 1,312 children aged 7-10. Reaction time variability (RTV) showed substantial genetic overlap with inattention, as observed in an additive genetic correlation of 0.64, compared to an additive genetic correlation of 0.31 with hyperactivity-impulsivity. Commission errors (CE) showed low additive genetic correlations with both hyperactivity-impulsivity and inattention (genetic correlations of 0.17 and 0.11, respectively). The additive genetic correlation between RTV and CE was also low and non-significant at -0.10, consistent with the etiological separation between the two indices of cognitive impairments. Overall, two key cognitive impairments phenotypically associated with ADHD symptoms, captured by RTV and CE, showed different genetic relationships to the two ADHD symptom domains. The findings extend a previous model of two familial cognitive impairment factors in combined subtype ADHD by separating pathways underlying inattention and hyperactivity-impulsivity symptoms.
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“These approaches have received clear support from aetiological studies indicating that most cases of ADHD arise from a 'pool' of genetic and environmental risk factors.”
From Attention-deficit/hyperactivity disorder (2015) · cites this paper as [33]
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“Neurocognitive, neuroimaging and genetic theories of ADHD have shifted from single-cause or singlepathway models to models that delineate causes that lead to ADHD through several molecular, neural and neurocognitive pathways 33,98-102 .”
From Attention-deficit/hyperactivity disorder (2015) · cites this paper as [33]
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“Family and twin studies have also demonstrated that genetic influences are shared between ADHD and a wide range of other neurodevelopmental and psycho pathological traits and disorders, including conduct disorder and problems 32 , cognitive performance 33 , autism s pectrum disorders 34 and mood disorders 35,36 .”
From Attention-deficit/hyperactivity disorder (2015) · cites this paper as [33]
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“Furthermore, hyperactivityimpulsivity decreases relative to inattention throughout development in both clinical (Biederman et al. 2000; Todd et al. 2008) and population (Larsson et al.”
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Distinct basal ganglia decision dynamics under conflict and uncertaintyPreprint
Ging-Jehli, N. R., Cavanagh, J. F., Ahn, M., Segar, D. J., Asaad, W. F., & Frank, M. J. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.09.12.612658
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Attention Deficit Hyperactivity Disorder: Genetics, Neural Networks, and Other Factors
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“Prior studies have theorized that there may be differing neural pathways to the disorder and unique genetic relationships within each symptom domain (Kuntsi et al., 2014 ; Sonuga-Barke, 2002 ).”
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Metadata
- Authors
- Kuntsi, J., Pinto, R., Price, T. S., van der Meere, J. J., Frazier-Wood, A. C., & Asherson, P.
- Affiliations
- King's College London (GB)
- Corresponding author
- Kuntsi, Jonna
- Venue
- Journal of Abnormal Child Psychology
- Published
- 2013-07-10
- Volume
- 42
- Issue
- 1
- Pages
- 127-136
- ISSN
- 0091-0627 (ISSN-L)
- 1573-2835
- PMC
- PMC4520068
- OpenAlex
- W2012675790
- Cited by
- 106
- References
- 46
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 9 · 2023: 6 · 2022: 8 · 2021: 10 · 2020: 13 · 2019: 8 · 2018: 13 · 2017: 1 · 2016: 11 · 2015: 9 · 2014: 9
- FWCI
- 6.84
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Research on Child and Adolescent Psychopathology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Research Portal (King's College London) (submittedVersion, other-oa)
- Research Portal (King's College London) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Funders
- Wellcome Trust (GR070345MF, 070345)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- attention deficit hyperactivity disorder, inattention, hyperactivity/impulsivity, genetic correlation, reaction time variability, commission errors, cognitive impairment, twin studies, children, go/no-go task
- MeSH terms
- Attention, Attention Deficit Disorder with Hyperactivity, Child, Cognition Disorders, Female, Humans, Impulsive Behavior, Male, Psychiatric Status Rating Scales, Reaction Time, Risk Factors, Twins, Comorbidity, Multivariate Analysis, Genetic Predisposition to Disease
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