ArticleTranslational psychiatry2016
Exome chip analyses in adult attention deficit hyperactivity disorder.
Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- A low frequency damaging SORCS2 variant identified in a family with ADHD compromises receptor stability and quenches activity.Molecular psychiatry · 2026Article
- Ge-SAND: an explainable deep learning-driven framework for disease risk prediction by uncovering complex genetic interactions in parallel.BMC genomics · 2025Article
- Psychiatric genetics in the diverse landscape of Latin American populations.Nature genetics · 2025Review
- Multi-omic analysis of the ciliogenic transcription factorbioRxiv : the preprint server for biology · 2025Article
- Increased burden of rare protein-truncating variants in constrained, brain-specific and synaptic genes in extremely impulsively violent males with antisocial personality disorder.Genes, brain, and behavior · 2024Article
- Characterization of genomic regions escaping epigenetic reprogramming in sheep.Environmental epigenetics · 2024Article
- Genetic architecture of ADHD and overlap with other psychiatric disorders and cognition-related phenotypes.Neuroscience and biobehavioral reviews · 2023Review
- Proteome-wide Identification of Off-Targets of a Potent EGFRACS medicinal chemistry letters · 2022Article
- Genome Guided Personalized Drug Therapy in Attention Deficit Hyperactivity Disorder.Frontiers in psychiatry · 2022Article
- The distinct roles of zinc finger CCHC-type (ZCCHC) superfamily proteins in the regulation of RNA metabolism.RNA biology · 2021Review
- GRASP55 restricts early-stage autophagy and regulates spatial organization of the early secretory network.Biology open · 2021Article
- Investigating cytosolic 5'-nucleotidase II family genes as candidates for neuropsychiatric disorders in Drosophila (114/150 chr).Translational psychiatry · 2021Article
- Article
- Identification of ADHD risk genes in extended pedigrees by combining linkage analysis and whole-exome sequencing.Molecular psychiatry · 2020Article
- Article
- Lipid-metabolizing serine hydrolases in the mammalian central nervous system: endocannabinoids and beyond.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Genetics of attention deficit hyperactivity disorder.Molecular psychiatry · 2019Review
- Live fast, die young? A review on the developmental trajectories of ADHD across the lifespan.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2018Review
- Novel Loci Associated With Attention-Deficit/Hyperactivity Disorder Are Revealed by Leveraging Polygenic Overlap With Educational Attainment.Journal of the American Academy of Child and Adolescent Psychiatry · 2018Article
- The SNP-set based association study identifies ITGA1 as a susceptibility gene of attention-deficit/hyperactivity disorder in Han Chinese.Translational psychiatry · 2017Article
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35 authors.
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Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a highly heritable childhood-onset neuropsychiatric condition, often persisting into adulthood. The genetic architecture of ADHD, particularly in adults, is largely unknown. We performed an exome-wide scan of adult ADHD using the Illumina Human Exome Bead Chip, which interrogates over 250 000 common and rare variants. Participants were recruited by the International Multicenter persistent ADHD CollaboraTion (IMpACT). Statistical analyses were divided into 3 steps: (1) gene-level analysis of rare variants (minor allele frequency (MAF)<1%); (2) single marker association tests of common variants (MAF⩾1%), with replication of the top signals; and (3) pathway analyses. In total, 9365 individuals (1846 cases and 7519 controls) were examined. Replication of the most associated common variants was attempted in 9847 individuals (2077 cases and 7770 controls) using fixed-effects inverse variance meta-analysis. With a Bonferroni-corrected significance level of 1.82E-06, our analyses of rare coding variants revealed four study-wide significant loci: 6q22.1 locus (P=4.46E-08), where NT5DC1 and COL10A1 reside; the SEC23IP locus (P=6.47E-07); the PSD locus (P=7.58E-08) and ZCCHC4 locus (P=1.79E-06). No genome-wide significant association was observed among the common variants. The strongest signal was noted at rs9325032 in PPP2R2B (odds ratio=0.81, P=1.61E-05). Taken together, our data add to the growing evidence of general signal transduction molecules (NT5DC1, PSD, SEC23IP and ZCCHC4) having an important role in the etiology of ADHD. Although the biological implications of these findings need to be further explored, they highlight the possible role of cellular communication as a potential core component in the development of both adult and childhood forms of ADHD.
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