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Network Toxicology Integrates In Vivo Evidence Linking Impaired Autophagic Clearance Involving the MTOR-TFEB Axis to Polystyrene Nanoplastic-Induced Neurotoxicity
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Scientists found that tiny plastic particles called nanoplastics, like those breaking down from everyday plastic products, can harm memory and learning in rats by disrupting the brain's natural "cleanup system" that clears out cellular waste. When this cleanup process breaks down, damaged material builds up in brain cells, contributing to cell death and cognitive problems. While this study was done in rats, it adds to growing evidence that plastic pollution may pose real risks to brain health, making it worth watching as scientists work out whether the same process happens in humans.
Long-term exposure to polystyrene nanoplastics (PS-NPs) causes neurotoxicity, but the underlying mechanisms remain unclear. We combined network toxicology, molecular docking, and in vivo experiments to investigate the role of MTOR-TFEB-regulated autophagy in PS-NP-induced neurotoxicity. Potential targets related to PS-NPs and neurodegenerative diseases were screened from public databases. Enrichment analysis indicated involvement of neurodegenerative and autophagy pathways. Protein–protein interaction and docking simulations prioritized MTOR as a candidate target. Sprague–Dawley rats were gavaged with PS-NPs (0.15 or 1.5 mg/kg) for 60 days. Morris water maze tests showed impaired spatial learning and memory. Western blotting of hippocampal tissues revealed increased p-MTOR/MTOR ratios, decreased total cytoplasmic and nuclear TFEB, reduced lysosomal proteins (LAMP2, CTSD, and CTSB), elevated autophagy markers SQSTM1 and MAP1LC3B-II, and altered apoptosis regulators (BAX up and BCL2 down). Collectively, PS-NPs disrupt the MTOR-TFEB axis, impair lysosomal function and autophagic clearance, and promote apoptosis, leading to neurocognitive deficits. These findings provide mechanistic insights into the MTOR-TFEB axis and highlight it as a candidate pathway warranting further evaluation as a potential intervention target.
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Polystyrene nanoplastics induced learning and memory impairments in mice by damaging the glymphatic system
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Mice exposed to polystyrene nanoplastics through different routes developed learning and memory problems linked to damage in their brain's waste-clearing system, called the glymphatic system. Amino-modified nanoplastics caused the most severe effects, disrupting the channels that normally flush toxins from the brain during sleep, suggesting a mechanism by which plastic pollution could contribute to cognitive decline.
Polystyrene nanoplastics induce cognitive dysfunction and dendritic spine deterioration via excessive mitochondrial fission
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Researchers demonstrated that polystyrene nanoplastics can cross the blood-brain barrier and accumulate in mouse brains, leading to cognitive impairment and loss of connections between brain cells. The damage was driven by excessive splitting of mitochondria, the energy-producing structures within cells, which triggered runaway cellular cleanup processes. Importantly, a drug that blocks this mitochondrial splitting reversed the cognitive damage, suggesting a potential therapeutic approach to nanoplastic-related brain injury.
Early-life exposure to polystyrene nanoplastics at ambient doses induces neurotoxicity via mTOR-mediated autophagy-lysosomal dysfunction and proteostasis imbalance
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Researchers exposed young mice to environmentally relevant doses of polystyrene nanoplastics and found that the particles penetrated their brains and caused behavioral and emotional disorders. The study identified a specific molecular mechanism in which nanoplastics disrupted the mTOR signaling pathway, leading to lysosomal dysfunction and a buildup of misfolded proteins that ultimately caused neurotoxicity. Treatments targeting these pathways were able to alleviate the harmful effects, suggesting potential avenues for intervention.
Deciphering the Neurotoxic Burden of Micro- and Nanoplastics: From Multi-model Experimental Evidence to Therapeutic Innovation
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This review summarizes research on how micro- and nanoplastics damage the brain and nervous system, covering evidence from cell studies, animal experiments, and clinical observations. Plastic particles can cross the blood-brain barrier, disrupt the gut-brain connection, cause oxidative stress, and trigger inflammation that leads to memory problems and cognitive decline. The review also discusses potential treatment strategies, making it a useful resource for understanding the brain health risks of plastic exposure.
Microglial clearance of Alzheimer's amyloid-beta obstructed by nanoplastics
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Researchers found that polystyrene nanoplastics interfere with the brain's ability to clear amyloid-beta, the protein that builds up in Alzheimer's disease. The nanoplastics accelerated amyloid clumping and drained the energy of brain immune cells that normally clean up these harmful proteins. This study suggests that nanoplastic exposure could worsen or contribute to the development of Alzheimer's disease.
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