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Peer-reviewedCC BY 4.0Advanced Science

Early‐Life Polyethylene Microplastic Exposure Exacerbates ADHD‐Like Behaviors in Mice via PI3K/AKT1/Nrf2 Signaling: Evidence From the Pilot Cohort and Multi‐Omics Analyses

  • Yufan Luo1,2
  • Ruijin Xie1,2
  • Hua Xu1,2
  • Xue Xiao1,2
  • Wei Xiao1,2
  • Qiyang Pan3,4
  • Shengjie Xu1,2
  • Li Liu5
  • Zeliang Xiao1,2
  • Yue Zhou1,2
  • Chenyu Sun4,6,7
  • Yu Wu2
1 more authors
  • Yueying Liu1
7 affiliations
  1. 1Department of Pediatrics Affiliated Hospital of Jiangnan University Wuxi Jiangsu China
  2. 2Lab of Modern Environmental Toxicology Public Health and Preventive Medicine Wuxi School of Medicine Jiangnan University Wuxi Jiangsu China
  3. 3Department of Psychiatry and Psychology Mayo Clinic Rochester Minnesota USA
  4. 4Mayo Clinic School of Graduate Medical Education Mayo Clinic College of Medicine and Science Rochester Minnesota USA
  5. 5Department of Internal Medicine The Second People's Hospital of Hefei Hefei Anhui China
  6. 6School of Public Health University of Minnesota‐Twin Cities Minneapolis USA
  7. 7Division of Public Health Infectious Diseases and Occupational Medicine Mayo Clinic Rochester Minnesota USA
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Abstract

Microplastic pollution may influence neurodevelopment, yet its relationship with attention‐deficit/hyperactivity disorder (ADHD) remains unclear. We integrated a pediatric cohort, multi‐omics analyses, network toxicology, and animal experiments to investigate polyethylene (PE) microplastic exposure in ADHD vulnerability. Among 90 children, PE was the predominant polymer detected in blood and was more abundant in children with ADHD. Higher PE burden was associated with greater symptom severity, increased IL‐6, and reduced antioxidant capacity. Multi‐omics and network analyses converged on PI3K/AKT1/Nrf2 signaling. In a perinatal nicotine mouse model, developmental PE co‐exposure exacerbated ADHD‐like behaviors, dopaminergic dysfunction, and oxidative injury. Melatonin partially alleviated these abnormalities by restoring PI3K/AKT1/GSK3β and Nrf2 signaling, whereas AAV‐mediated PI3K knockdown weakened its protective effects. Collectively, the human findings identify circulating PE burden as an environmental correlate of ADHD‐related neurodevelopmental vulnerability, while the animal experiments provide evidence that developmental PE co‐exposure can aggravate ADHD‐like abnormalities in a susceptible background.

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Cite

BibTeXRIS
BibTeX
@article{luo2026earlylife,
  title = {{Early‐Life Polyethylene Microplastic Exposure Exacerbates ADHD‐Like Behaviors in Mice via PI3K/AKT1/Nrf2 Signaling: Evidence From the Pilot Cohort and Multi‐Omics Analyses}},
  author = {Yufan Luo and Ruijin Xie and Hua Xu and Xue Xiao and Wei Xiao and Qiyang Pan and Shengjie Xu and Li Liu and Zeliang Xiao and Yue Zhou and Chenyu Sun and Yu Wu and Yueying Liu},
  journal = {Advanced Science},
  year = {2026},
  month = nov,
  doi = {10.1002/advs.78594},
  url = {https://doi.org/10.1002/advs.78594},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Early‐Life Polyethylene Microplastic Exposure Exacerbates ADHD‐Like Behaviors in Mice via PI3K/AKT1/Nrf2 Signaling: Evidence From the Pilot Cohort and Multi‐Omics Analyses
AU  - Yufan Luo
AU  - Ruijin Xie
AU  - Hua Xu
AU  - Xue Xiao
AU  - Wei Xiao
AU  - Qiyang Pan
AU  - Shengjie Xu
AU  - Li Liu
AU  - Zeliang Xiao
AU  - Yue Zhou
AU  - Chenyu Sun
AU  - Yu Wu
AU  - Yueying Liu
PY  - 2026
DA  - 2026/11/01
JO  - Advanced Science
DO  - 10.1002/advs.78594
UR  - https://doi.org/10.1002/advs.78594
AB  - Microplastic pollution may influence neurodevelopment, yet its relationship with attention‐deficit/hyperactivity disorder (ADHD) remains unclear. We integrated a pediatric cohort, multi‐omics analyses, network toxicology, and animal experiments to investigate polyethylene (PE) microplastic exposure in ADHD vulnerability. Among 90 children, PE was the predominant polymer detected in blood and was more abundant in children with ADHD. Higher PE burden was associated with greater symptom severity, increased IL‐6, and reduced antioxidant capacity. Multi‐omics and network analyses converged on PI3K/AKT1/Nrf2 signaling. In a perinatal nicotine mouse model, developmental PE co‐exposure exacerbated ADHD‐like behaviors, dopaminergic dysfunction, and oxidative injury. Melatonin partially alleviated these abnormalities by restoring PI3K/AKT1/GSK3β and Nrf2 signaling, whereas AAV‐mediated PI3K knockdown weakened its protective effects. Collectively, the human findings identify circulating PE burden as an environmental correlate of ADHD‐related neurodevelopmental vulnerability, while the animal experiments provide evidence that developmental PE co‐exposure can aggravate ADHD‐like abnormalities in a susceptible background.
SN  - 2198-3844
ER  -