The short version
Demontis and colleagues reported 27 genome-wide significant ADHD risk regions in a 2023 analysis of 38,691 cases and 186,843 controls. Each row below is a region anchored by an index variant, not a confirmed causal gene or a diagnostic result. The paper reports 32 independent lead variants across these 27 regions; this guide follows its Table 1, one entry per region [1].
A different 2025 analysis incorporating childhood symptom scores reported 39 loci under its own study design. The counts should not be added together or read as a simple time series. See GEN-01 for the broader context [2].
How to use the locus links
Select a locus in the index to jump to its entry. Chromosome positions use the paper’s hg19 reference assembly. The listed genes are within 50 kb of the index variant in Table 1; an empty cell means that table listed none in that window. The odds ratio is for effect allele A1, comparing alleles in this study, and is not an individual prediction. P values describe association evidence, not the size or clinical meaning of an effect [1].
Locus index
| Locus | Index variant | Chromosome and hg19 position | Nearby genes within 50 kb |
|---|---|---|---|
| Locus 01 | rs549845 | 1:44,076,469 | PTPRF, KDM4A |
| Locus 02 | rs1438898 | 2:145,714,354 | None listed |
| Locus 03 | rs2886697 | 3:20,724,204 | None listed |
| Locus 04 | rs9877066 | 3:43,691,501 | SNRK, ANO10, ABHD5 |
| Locus 05 | rs7613360 | 3:49,916,710 | TRAIP, CAMKV, MST1R, CTD-2330K9.3, MON1A |
| Locus 06 | rs2311059 | 3:51,884,072 | IQCF3, IQCF2, IQCF5, IQCF1 |
| Locus 07 | rs17718444 | 3:71,499,401 | FOXP1 |
| Locus 08 | rs114142727 | 3:87,015,142 | VGLL3 |
| Locus 09 | rs17576773 | 4:112,217,523 | None listed |
| Locus 10 | rs6537401 | 4:147,099,654 | LSM6, RP11-6L6.2, SLC10A7 |
| Locus 11 | rs4916723 | 5:87,854,395 | None listed |
| Locus 12 | rs77960 | 5:103,964,585 | None listed |
| Locus 13 | rs10875612 | 5:144,474,779 | None listed |
| Locus 14 | rs2025286 | 6:70,858,701 | COL19A1 |
| Locus 15 | rs73145587 | 7:67,685,754 | None listed |
| Locus 16 | rs9969232 | 7:114,158,954 | FOXP2 |
| Locus 17 | rs7844069 | 8:93,277,087 | None listed |
| Locus 18 | rs4925811 | 8:145,802,447 | C8orf82, ARHGAP39 |
| Locus 19 | rs11255890 | 10:8,784,773 | None listed |
| Locus 20 | rs11596214 | 10:106,453,832 | SORCS3 |
| Locus 21 | rs2582895 | 11:28,602,173 | METTL15 |
| Locus 22 | rs704061 | 12:89,771,903 | DUSP6, POC1B |
| Locus 23 | rs76284431 | 14:98,690,923 | None listed |
| Locus 24 | rs1162202 | 16:61,966,703 | CDH8 |
| Locus 25 | rs76857496 | 18:5,871,800 | TMEM200C |
| Locus 26 | rs7506904 | 18:50,625,779 | DCC |
| Locus 27 | rs6082363 | 20:21,250,843 | XRN2, NKX2-4 |
The 27 regions in detail
Locus 01
Index variant: rs549845 · Position: chromosome 1, hg19 44,076,469 · A1/A2: G/A · Odds ratio for A1: 1.082 · P: 9.03e-15 [1].
Genes within 50 kb in Table 1: PTPRF, KDM4A. Previously reported relative to the 2019 GWAS.
The authors highlight PTPRF among candidate postsynaptic-density genes. That is pathway context, not proof that PTPRF rather than another mapped gene mediates this association.
Locus 02
Index variant: rs1438898 · Position: chromosome 2, hg19 145,714,354 · A1/A2: A/C · Odds ratio for A1: 1.065 · P: 4.88e-9 [1].
Genes within 50 kb in Table 1: None listed. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 03
Index variant: rs2886697 · Position: chromosome 3, hg19 20,724,204 · A1/A2: G/A · Odds ratio for A1: 1.061 · P: 7.90e-10 [1].
Genes within 50 kb in Table 1: None listed. Previously reported relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 04
Index variant: rs9877066 · Position: chromosome 3, hg19 43,691,501 · A1/A2: G/A · Odds ratio for A1: 0.888 · P: 6.60e-9 [1].
Genes within 50 kb in Table 1: SNRK, ANO10, ABHD5. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 05
Index variant: rs7613360 · Position: chromosome 3, hg19 49,916,710 · A1/A2: C/T · Odds ratio for A1: 0.948 · P: 3.18e-8 [1].
Genes within 50 kb in Table 1: TRAIP, CAMKV, MST1R, CTD-2330K9.3, MON1A. New relative to the 2019 GWAS.
This chromosome 3 signal sits near several genes, which is precisely why a single nearest-gene explanation would be premature. Compare the authors' fine-mapping and functional mapping before naming a target.
Locus 06
Index variant: rs2311059 · Position: chromosome 3, hg19 51,884,072 · A1/A2: G/A · Odds ratio for A1: 0.944 · P: 3.16e-8 [1].
Genes within 50 kb in Table 1: IQCF3, IQCF2, IQCF5, IQCF1. New relative to the 2019 GWAS.
This is a separate chromosome 3 locus close to locus 5 on a chromosome-scale figure. Physical proximity on a plot does not merge the two index-variant records.
Locus 07
Index variant: rs17718444 · Position: chromosome 3, hg19 71,499,401 · A1/A2: C/T · Odds ratio for A1: 1.063 · P: 2.87e-9 [1].
Genes within 50 kb in Table 1: FOXP1. New relative to the 2019 GWAS.
FOXP1 is a transcription-factor gene. The paper reports a signal in its transcribed region and credible variants in brain chromatin-interacting regions. Rare FOXP1 disorders are a different type of evidence from this common-variant ADHD association.
Locus 08
Index variant: rs114142727 · Position: chromosome 3, hg19 87,015,142 · A1/A2: C/G · Odds ratio for A1: 1.285 · P: 5.13e-10 [1].
Genes within 50 kb in Table 1: VGLL3. New relative to the 2019 GWAS.
The effect allele (C) is the common one here, at a frequency of about 0.99 in both cases and controls; the other allele is rare. Its reported odds ratio is larger than those of most rows. An association estimate is not a clinical penetrance estimate.
Locus 09
Index variant: rs17576773 · Position: chromosome 4, hg19 112,217,523 · A1/A2: C/T · Odds ratio for A1: 1.101 · P: 1.63e-10 [1].
Genes within 50 kb in Table 1: None listed. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 10
Index variant: rs6537401 · Position: chromosome 4, hg19 147,099,654 · A1/A2: G/A · Odds ratio for A1: 0.945 · P: 1.40e-8 [1].
Genes within 50 kb in Table 1: LSM6, RP11-6L6.2, SLC10A7. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 11
Index variant: rs4916723 · Position: chromosome 5, hg19 87,854,395 · A1/A2: A/C · Odds ratio for A1: 0.918 · P: 9.48e-15 [1].
Genes within 50 kb in Table 1: None listed. Previously reported relative to the 2019 GWAS.
The main text describes this strong chromosome 5 signal as downstream of MEF2C; the Table 1 nearby-gene cell is blank under its 50 kb rule. A downstream label does not make MEF2C a proven causal gene.
Locus 12
Index variant: rs77960 · Position: chromosome 5, hg19 103,964,585 · A1/A2: G/A · Odds ratio for A1: 0.929 · P: 2.46e-13 [1].
Genes within 50 kb in Table 1: None listed. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 13
Index variant: rs10875612 · Position: chromosome 5, hg19 144,474,779 · A1/A2: C/T · Odds ratio for A1: 0.947 · P: 5.62e-9 [1].
Genes within 50 kb in Table 1: None listed. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 14
Index variant: rs2025286 · Position: chromosome 6, hg19 70,858,701 · A1/A2: A/C · Odds ratio for A1: 0.947 · P: 4.00e-9 [1].
Genes within 50 kb in Table 1: COL19A1. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 15
Index variant: rs73145587 · Position: chromosome 7, hg19 67,685,754 · A1/A2: A/T · Odds ratio for A1: 1.107 · P: 3.67e-8 [1].
Genes within 50 kb in Table 1: None listed. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 16
Index variant: rs9969232 · Position: chromosome 7, hg19 114,158,954 · A1/A2: G/A · Odds ratio for A1: 0.934 · P: 9.98e-12 [1].
Genes within 50 kb in Table 1: FOXP2. Previously reported relative to the 2019 GWAS.
The paper highlights FOXP2 alongside FOXP1. Credible variants at FOXP2 were linked to brain eQTL information; this still leaves the variant-to-gene causal chain to test.
Locus 17
Index variant: rs7844069 · Position: chromosome 8, hg19 93,277,087 · A1/A2: T/G · Odds ratio for A1: 1.057 · P: 6.74e-9 [1].
Genes within 50 kb in Table 1: None listed. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 18
Index variant: rs4925811 · Position: chromosome 8, hg19 145,802,447 · A1/A2: T/G · Odds ratio for A1: 0.944 · P: 8.30e-9 [1].
Genes within 50 kb in Table 1: C8orf82, ARHGAP39. New relative to the 2019 GWAS.
ARHGAP39 appears among the genes mapped to synaptic annotations and early developmental expression in the study. Those are gene-set observations, not direct functional validation of this index variant.
Locus 19
Index variant: rs11255890 · Position: chromosome 10, hg19 8,784,773 · A1/A2: C/A · Odds ratio for A1: 1.054 · P: 4.14e-8 [1].
Genes within 50 kb in Table 1: None listed. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 20
Index variant: rs11596214 · Position: chromosome 10, hg19 106,453,832 · A1/A2: G/A · Odds ratio for A1: 1.054 · P: 3.17e-8 [1].
Genes within 50 kb in Table 1: SORCS3. Previously reported relative to the 2019 GWAS.
SORCS3 received additional attention: in the study's own exome data, its rare protein-truncating variant burden was nominally significant within a larger gene set, which the authors describe as potentially implicating the gene. The authors describe common–rare convergence as suggestive, not a definitive single-gene diagnosis.
Locus 21
Index variant: rs2582895 · Position: chromosome 11, hg19 28,602,173 · A1/A2: C/A · Odds ratio for A1: 1.075 · P: 4.09e-14 [1].
Genes within 50 kb in Table 1: METTL15. New relative to the 2019 GWAS.
This chromosome 11 region was one of the three strongest associations and was described as downstream of METTL15. The nearby-gene label does not establish METTL15 as the causal mediator.
Locus 22
Index variant: rs704061 · Position: chromosome 12, hg19 89,771,903 · A1/A2: T/C · Odds ratio for A1: 0.946 · P: 2.30e-9 [1].
Genes within 50 kb in Table 1: DUSP6, POC1B. Previously reported relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 23
Index variant: rs76284431 · Position: chromosome 14, hg19 98,690,923 · A1/A2: T/A · Odds ratio for A1: 0.922 · P: 1.19e-9 [1].
Genes within 50 kb in Table 1: None listed. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 24
Index variant: rs1162202 · Position: chromosome 16, hg19 61,966,703 · A1/A2: C/T · Odds ratio for A1: 1.063 · P: 1.92e-9 [1].
Genes within 50 kb in Table 1: CDH8. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 25
Index variant: rs76857496 · Position: chromosome 18, hg19 5,871,800 · A1/A2: C/A · Odds ratio for A1: 1.083 · P: 1.24e-8 [1].
Genes within 50 kb in Table 1: TMEM200C. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
Locus 26
Index variant: rs7506904 · Position: chromosome 18, hg19 50,625,779 · A1/A2: G/A · Odds ratio for A1: 0.946 · P: 1.24e-8 [1].
Genes within 50 kb in Table 1: DCC. New relative to the 2019 GWAS.
DCC is among the study's postsynaptic-density candidates. This supplies a plausible biological lead, while the index association alone cannot choose among linked variants or mechanisms.
Locus 27
Index variant: rs6082363 · Position: chromosome 20, hg19 21,250,843 · A1/A2: T/C · Odds ratio for A1: 1.073 · P: 4.38e-12 [1].
Genes within 50 kb in Table 1: XRN2, NKX2-4. New relative to the 2019 GWAS.
The table reports a robust regional association. It does not resolve the causal variant, target gene, cell type or individual effect. Functional mapping is a separate evidence step.
The usual mix-up
A nearby gene is a location clue, not an identified mechanism. A small odds ratio also does not say whether a person has ADHD or whether they need care. The evidence for assessment and timely support is clinical and functional, alongside the biological evidence; no one needs a genetic result to seek care. See GEN-02 and the site’s care and rights pages.
The deeper layer (optional to read)
A GWAS tests associations across many markers. Linkage disequilibrium means the index variant may tag another causal variant; regulatory effects may reach genes outside the 50 kb column. The paper used additional mapping and functional analyses to prioritise possible genes, but those analyses are a different kind of evidence from Table 1. Its 76 prioritised genes are candidates rather than 76 confirmed causes [1].
The row for locus 11 has no gene in the 50 kb table cell, although the authors discuss its relationship to MEF2C downstream. Locus 20 also has nominal rare-variant evidence around SORCS3 from the study's exome data. These details are reasons to examine the paper’s follow-up analysis, not to relabel every row with a single causal gene [1].
Limits
This is a guide to one historical study’s table, not a current count of all ADHD loci. The study population and analytic choices limit how directly any estimate transfers across ancestries or to an individual. Neither the index variant nor the listed nearby gene is a clinical test or treatment selector. The author correction to the paper fixed a misspelled author name and an omitted acknowledgement, and does not change Table 1; consult the linked correction alongside the study [1, 3].
Sources
- Demontis D et al. Genome-wide analyses of ADHD identify 27 risk loci, refine the genetic architecture and implicate several cognitive domains. Nature Genetics 2023. DOI · PMID 36702997. Table 1 and discussion.
- van der Laan CM et al. Genome-wide association meta-analysis of childhood ADHD symptoms and diagnosis identifies new loci and potential effector genes. Nature Genetics 2025. DOI · PMID 40962958.
- Demontis D et al. Author Correction. Nature Genetics 2023. DOI.