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Application of brain organoid technology in exploring the neurotoxicity of micro/nanoplastics: a review of progress and challenges
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A review of brain organoid studies found that micro- and nanoplastics can penetrate these human-derived tissue models and cause mitochondrial dysfunction, calcium signaling disruption, and abnormal neural differentiation resembling neurodegenerative pathology. This significantly advances microplastic pollution research by establishing brain organoids as an ethical and translationally relevant model for assessing the neurotoxic risks of environmental plastic exposure in humans.
As an emerging environmental pollutant, micro/nanoplastics (MNPs) have been reported to accumulate in brain tissues, which may lead to risks of neurotoxicity in humans. Current traditional neurotoxicity models face difficulties in species differences and ethical limitations, whereas brain organoids derived from human cells can simulate the complex structure and function of the human brain, providing a novel model for studying the neurotoxicity of MNPs. In this study, we have reviewed the progress in applying brain organoids to assess the health risks of environmental pollutants including MNPs. MNPs can penetrate into brain organoids and cause toxic effects such as mitochondrial dysfunction, calcium signaling disruption, and abnormal neural differentiation, which may promote pathological phenotypes associated with neurodegenerative diseases. These findings are usually obtained from organoids derived from human-induced pluripotent stem cells, whereas models derived from human embryonic stem cells still require further exploration. Future perspectives are also proposed for technological innovation in brain organoids, including developing region-specific brain organoids, fetal brain organoids, and standardized brain organoid platforms to facilitate their broader application in environmental neurotoxicity assessment of environmental pollutants.
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