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Background <p>Attention-Deficit/Hyperactivity Disorder (ADHD) is a highly prevalent neurodevelopmental disorder with complex biological underpinnings involving genetic, neuroimaging, and environmental factors. Despite extensive research, a unified quantitative synthesis integrating these domains remains limited.</p> Methods <p>A systematic umbrella review was conducted following PRISMA 2020 guidelines. Four databases (PubMed, Web of Science, Scopus, PsycINFO) were searched up to March 2026. Eligible studies were meta-analyses or mega-analyses reporting quantitative effect sizes related to ADHD biological mechanisms. This review was not prospectively registered in a public database (e.g., PROSPERO).</p> Results <p>Ten high-quality studies encompassing over 4.6 million participants were included. ADHD demonstrated high heritability (h<sup>2</sup> ≈ 0.74), with a notable gap between twin-based and SNP-based estimates. Neuroimaging findings revealed consistent but modest structural and functional alterations, particularly in fronto-striatal and default mode networks. Environmental factors, including prenatal tobacco exposure, lead, and air pollution, showed significant associations with ADHD risk.</p> Conclusions <p>ADHD arises from the interaction of polygenic vulnerability and environmental exposures, converging on catecholaminergic dysregulation in fronto-striatal circuits. While genetic and neuroimaging markers show small individual effects, environmental factors present modifiable targets for prevention. These findings support a unified multi-level biological model of ADHD.</p>

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Integrating genetics, neuroimaging, and environment in ADHD: a systematic umbrella review of meta-analytic evidence

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月26日

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  • Mukhayo Khayitboeva,
  • Hayot Yuldosheva,
  • Yulduz Nishanova,
  • Nasiba Normatova,
  • Malikakhon Aripkhodzhaeva,
  • Mokhinur Khamidova

摘要

Background

Attention-Deficit/Hyperactivity Disorder (ADHD) is a highly prevalent neurodevelopmental disorder with complex biological underpinnings involving genetic, neuroimaging, and environmental factors. Despite extensive research, a unified quantitative synthesis integrating these domains remains limited.

Methods

A systematic umbrella review was conducted following PRISMA 2020 guidelines. Four databases (PubMed, Web of Science, Scopus, PsycINFO) were searched up to March 2026. Eligible studies were meta-analyses or mega-analyses reporting quantitative effect sizes related to ADHD biological mechanisms. This review was not prospectively registered in a public database (e.g., PROSPERO).

Results

Ten high-quality studies encompassing over 4.6 million participants were included. ADHD demonstrated high heritability (h2 ≈ 0.74), with a notable gap between twin-based and SNP-based estimates. Neuroimaging findings revealed consistent but modest structural and functional alterations, particularly in fronto-striatal and default mode networks. Environmental factors, including prenatal tobacco exposure, lead, and air pollution, showed significant associations with ADHD risk.

Conclusions

ADHD arises from the interaction of polygenic vulnerability and environmental exposures, converging on catecholaminergic dysregulation in fronto-striatal circuits. While genetic and neuroimaging markers show small individual effects, environmental factors present modifiable targets for prevention. These findings support a unified multi-level biological model of ADHD.