To link identified risk variants to genes, we first identified sets of Bayesian credible variants for each risk locus, with each set most likely (probability > 95%) including a causal variant (Supplementary Table 6). Credible variants were subsequently linked to genes based on genomic position, information about expression quantitative trait loci (eQTLs) and chromatin interaction mapping in human brain tissue as implemented in FUMA23 (datasets selected are listed in the Supplementary Note). We identified 76 plausible ADHD risk genes (Supplementary Table 7); four of the 76 were mapped by position alone. We found that this set of genes is significantly enriched among genes upregulated during early embryonic brain development (19th post-conceptual week; Pone_sided = 0.0008; Supplementary Fig. 3) and highly enriched for genes identified in GWASs of cognition-related phenotypes and reproduction (Supplementary Fig. 4). The role of the genes in synapses was evaluated using SynGO data24; nine genes mapped to SynGO annotations, and genes encoding integral components of the postsynaptic density membrane were borderline significantly enriched (P = 5.43 × 10−3; q-value 0.022; genes PTPRF, SORCS3, and DCC; Supplementary Fig.
