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Related Concept Videos

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Attention-Deficit/Hyperactivity Disorder

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Diagnostic Criteria and Symptoms
To diagnose ADHD, symptoms must manifest before age 12 and be evident across multiple settings.
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Related Experiment Video

Updated: Jun 17, 2026

Using Brain Activation (nir-HEG/Q-EEG) and Execution Measures (CPTs) in a ADHD Assessment Protocol
13:09

Using Brain Activation (nir-HEG/Q-EEG) and Execution Measures (CPTs) in a ADHD Assessment Protocol

Published on: April 1, 2018

Shared genetic architecture between ADHD and intelligence varies across ADHD subtypes.

Qiyu Zhao1, Kun Yang2, Mengge Liu3

  • 1Department of Radiology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.

BMC Medicine
|June 16, 2026
PubMed
Summary

Genetic studies reveal that the shared genetic basis between attention-deficit/hyperactivity disorder (ADHD) and intelligence differs across ADHD subtypes. These findings highlight distinct biological pathways and inform early identification strategies.

Keywords:
ADHD subtypesgeneral cognitive abilitygenetic architectureintelligencepolygenic overlap

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12:21

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Area of Science:

  • Neurogenetics
  • Psychiatric Genetics
  • Cognitive Neuroscience

Background:

  • Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental condition with significant cognitive comorbidities.
  • Previous genetic research indicates overlap between ADHD and intelligence, but often treats ADHD as a singular entity.
  • The genetic architecture shared across different ADHD subtypes and intelligence remains largely unexplored.

Purpose of the Study:

  • To investigate the shared genetic architecture between ADHD, its subtypes (childhood, persistent, late-diagnosed), and intelligence.
  • To characterize the nature of genetic overlap, including genome-wide correlations, polygenic overlap, and variant-level associations.
  • To identify specific genetic loci and biological pathways underlying the relationship between ADHD subtypes and intelligence.

Main Methods:

  • Genome-wide cross-trait analyses integrating large-scale GWAS data for ADHD phenotypes and intelligence (N > 300,000).
  • Evaluation of genome-wide genetic correlations, polygenic overlap, local genetic correlations, and variant-level associations.
  • Identification and functional annotation of shared genetic loci, followed by gene-set enrichment analyses.
  • Two-sample Mendelian randomization to assess bidirectional causal relationships, with sensitivity analyses and validation in independent GWAS datasets.

Main Results:

  • Significant negative genetic correlations were observed between all ADHD phenotypes and intelligence (rg: -0.3442 to -0.4205).
  • Substantial genetic overlap was identified, including 184 jointly associated loci (64 novel), with no shared loci found for persistent ADHD.
  • Functional annotation revealed distinct pathway enrichments: childhood ADHD loci linked to early neurodevelopment, late-diagnosed ADHD loci to synaptic and neuronal signaling.
  • Mendelian randomization suggested a bidirectional association, with stronger evidence for intelligence influencing ADHD risk; findings were robust across validation datasets.

Conclusions:

  • The genetic architecture linking ADHD and intelligence is subtype-specific, indicating distinct biological underpinnings for cognitive heterogeneity in ADHD.
  • The relationship between ADHD liability and general cognitive ability is not uniform across subtypes.
  • These findings have implications for risk stratification and early identification in child and adolescent psychiatry.