Polygenic risk score
Attention-Deficit / Hyperactivity Disorder (ADHD)
ICD-11 6A05 · Neurodevelopmental
The ADHD polygenic risk score summarizes your cumulative common-variant liability for Attention-Deficit/Hyperactivity Disorder, drawn from the largest published genome-wide association study of the condition. It is a population statistic — not a diagnosis, and not a destiny.
Polygenic risk scores for ADHD explain roughly 5.5% of variance in liability in European-ancestry validation samples — informative at population scale, but not diagnostic at the individual level.
At a glance
ADHD is a highly heritable neurodevelopmental condition with well-replicated genetic risk variants. Your score reflects the cumulative effect of common variants linked to ADHD in the largest published GWAS to date.
Attention-Deficit/Hyperactivity Disorder is a common neurodevelopmental condition involving inattention, hyperactivity, and impulsivity. Twin studies consistently estimate heritability around 70-80%. The 2022 Psychiatric Genomics Consortium GWAS analyzed ~225,000 individuals and identified 27 genome-wide significant loci — the variants we score below.
What the GWAS actually found
The 2023 PGC meta-analysis (Demontis et al., Nature Genetics) combined 38,691 ADHD cases and 186,843 controls across cohorts spanning childhood and adult ADHD. It identified 27 independent loci reaching genome-wide significance and estimated SNP-based heritability at approximately 22%. A top-hit gene named in the paper is SORCS3, which encodes a sorting receptor with a role in synaptic plasticity.
Twin studies place total heritability for ADHD at 0.70–0.80 in childhood and 0.50–0.60 in adulthood. The gap between twin-study heritability and SNP-based heritability reflects the contribution of rare variants, copy-number variants, and gene–environment interactions that a common-variant PRS cannot capture.
How to read your percentile
Below 25th
Lower common-variant liability than most of the reference cohort. Does not rule out ADHD — environment and rare variants still contribute.
25th–75th
Typical range. Your score is close to the population average; this signal is uninformative for individual risk prediction.
Above 75th
Elevated common-variant liability. Interpret as an incremental probabilistic signal, not a diagnosis. PRS adds modest discrimination on top of clinical and environmental factors.
What this does not tell you
An ADHD PRS cannot diagnose ADHD, predict whether symptoms will emerge in a person who does not have them, or identify a specific ADHD subtype. Clinical diagnosis requires evaluation by a qualified clinician and depends on observed symptomatology, functional impairment, and age of onset — not genetics.
The score is built from common variants only. Rare single-nucleotide variants and copy-number variants at loci such as 15q11.2 and 16p13.11 meaningfully elevate ADHD risk in carriers and are invisible to this analysis. The PGC cohort is predominantly European-ancestry; accuracy typically drops 30–70% in non-European populations.
Related traits
Attention-Deficit / Hyperactivity Disorder (ADHD) shares common-variant architecture with several other psychiatric conditions. Genetic correlations (rg) reflect how often the same variants move risk for both traits in the same direction.
Frequently asked questions
Can a polygenic risk score predict whether I will develop ADHD?
No. A PRS summarizes common-variant genetic liability at the population level. It cannot diagnose ADHD or determine whether you will develop it. Environmental exposures, rare variants, and structural variants (CNVs) all contribute to ADHD risk and are not captured in a common-variant PRS.
How accurate is the ADHD polygenic risk score?
The ADHD PRS built from PGC 2022 summary statistics explains approximately 5.5% of variance in liability (R² on the liability scale) in European-ancestry validation samples. Accuracy drops substantially in non-European ancestries — typically by 30–70% depending on population.
Does the score apply the same way to children and adults?
The PGC 2022 meta-analysis combined childhood and adult ADHD cohorts, and the resulting PRS has been validated in both. Twin-study heritability is slightly higher in children (~0.74) than in adults (~0.50–0.60), but the common-variant PRS captures shared genetic liability across the lifespan.
What about rare variants and copy-number variants?
A common-variant PRS does not capture rare single-nucleotide variants or CNVs. Large CNVs at loci like 15q11.2 and 16p13.11 meaningfully elevate ADHD risk in carriers and are invisible to array-based PRS scoring.
Sources
- Demontis et al. 2023, Nature Genetics 55:198–208. doi.org/10.1038/s41588-022-01285-8
- PGC ADHD Working Group. pgc.unc.edu/for-researchers/working-groups/adhd-workgroup/
- Faraone & Larsson 2019 — Genetics of ADHD. doi.org/10.1038/s41380-018-0070-0
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