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<p>With the intensification of global plastic pollution, the potential threats posed by micro- and nanoplastics (MPs/NPs) to human health have become a major concern. MPs/NPs enter the organism through ingestion, inhalation, and skin contact, subsequently accumulating in multiple organs—particularly the brain. Increasing experimental and epidemiological evidence implicates MPs/NPs in the development of Parkinson’s disease (PD). Preclinical research models indicate that MPs/NPs may accelerate both the initiation and progression of PD by facilitating α-synuclein misfolding and aggregation, triggering neuroinflammatory cascades, elevating oxidative stress, and impairing mitochondrial function. To further investigate the causal role of MPs/NPs in PD, upcoming studies should emphasize well-designed, large-scale prospective cohorts to assess individual exposure to plastic-related pollutants, elucidate the pathways of MPs/NPs into the central nervous system, establish safety thresholds for their neurotoxicity, explore the correlation between exposure levels and central nervous system accumulation, clarify the temporal relationship between MPs/NPs accumulation and PD pathology and symptom onset, and identify the neuropathological mechanisms triggered by relevant concentrations of MPs/NPs. Such data will be instrumental in informing preventive and potentially interventional strategies, while offering actionable insights into the interaction between MPs/NPs and PD.</p>

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Micro-nanoplastics and Parkinson’s disease: evidence and perspectives

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月24日

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  • Lu Lin,
  • Jin Li,
  • Si Zhu,
  • Zhiling Zhang,
  • Zhigang Li,
  • Pingyi Xu,
  • Wenyuan Guo

摘要

With the intensification of global plastic pollution, the potential threats posed by micro- and nanoplastics (MPs/NPs) to human health have become a major concern. MPs/NPs enter the organism through ingestion, inhalation, and skin contact, subsequently accumulating in multiple organs—particularly the brain. Increasing experimental and epidemiological evidence implicates MPs/NPs in the development of Parkinson’s disease (PD). Preclinical research models indicate that MPs/NPs may accelerate both the initiation and progression of PD by facilitating α-synuclein misfolding and aggregation, triggering neuroinflammatory cascades, elevating oxidative stress, and impairing mitochondrial function. To further investigate the causal role of MPs/NPs in PD, upcoming studies should emphasize well-designed, large-scale prospective cohorts to assess individual exposure to plastic-related pollutants, elucidate the pathways of MPs/NPs into the central nervous system, establish safety thresholds for their neurotoxicity, explore the correlation between exposure levels and central nervous system accumulation, clarify the temporal relationship between MPs/NPs accumulation and PD pathology and symptom onset, and identify the neuropathological mechanisms triggered by relevant concentrations of MPs/NPs. Such data will be instrumental in informing preventive and potentially interventional strategies, while offering actionable insights into the interaction between MPs/NPs and PD.