Annual Research Review: Perspectives on progress in ADHD science – from characterization to cause
Edmund J. S. Sonuga-Barke, Stephen P. Becker, Sven Bölte, F. Xavier Castellanos, Barbara Franke, Jeffrey H. Newcorn et al. · 2022 · 150 citationsRead the paper
The science of attention-deficit/hyperactivity disorder (ADHD) is motivated by a translational goal - the discovery and exploitation of knowledge about the nature of ADHD to the benefit of those individuals whose lives it affects. Over the past fifty years, scientific research has made enormous strides in characterizing the ADHD condition and in understanding its correlates and causes. However, the translation of these scientific insights into clinical benefits has been limited. In this review, we provide a selective and focused survey of the scientific field of ADHD, providing our personal perspectives on what constitutes the scientific consensus, important new leads to be highlighted, and the key outstanding questions to be addressed going forward. We cover two broad domains - clinical characterization and, risk factors, causal processes and neuro-biological pathways. Part one focuses on the developmental course of ADHD, co-occurring characteristics and conditions, and the functional impact of living with ADHD - including impairment, quality of life, and stigma. In part two, we explore genetic and environmental influences and putative mediating brain processes. In the final section, we reflect on the future of the ADHD construct in the light of cross-cutting scientific themes and recent conceptual reformulations that cast ADHD traits as part of a broader spectrum of neurodivergence.
What the full text shows
Shown in the lab- Twin studies show high heritability of ADHD, while genome-wide studies of common variants show significantly lower estimates. — 74% (twin studies) vs. 20–30% (genome-wide studies)
- Polygenic risk scores derived from GWAS explain a small fraction of ADHD variance. — ~3% of variance (ADHD broadly defined)
- Large-scale neuroimaging (ENIGMA) shows ADHD-related brain alterations are smaller than previously reported. — Cohen’s d < 0.20 (Childhood samples (~3,200 to ~4,200 participants))
- Community-ascertained samples (ABCD) show even smaller structural brain differences than clinical samples. — d = -0.08 for total intracranial volume and total cortical surface area (Children aged 9-10 years (n ≈ 11,700))
- Mendelian Randomization suggests ADHD is causal for lifetime cannabis use.
- Genetic liability for ADHD affects educational attainment independently of general cognitive ability.
- Setup
- Review of multiple datasets including ENIGMA (3,200-4,200 participants) and ABCD (~11,700 children).
- How
- The authors conducted a selective survey and review of existing scientific literature, synthesizing findings from twin studies, GWAS, large-scale neuroimaging consortia (ENIGMA, ABCD), and Mendelian Randomization studies.
- Limitations
- Small effect sizes of individual genetic and environmental risk factors. · Inconsistency in neuroimaging results due to head motion artifacts and sample size. · Difficulty translating in vitro or animal neurochemistry findings to humans. · Discrepancy between twin-based and molecular genetic heritability estimates.
Summarized by Gemma 4 from the open-access full text · 9 Oct 2026. Read it