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Adolescent exposure to micro/nanoplastics induces cognitive impairments in mice with neuronal morphological damage and multi-omic alterations
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Adolescent mice exposed to polystyrene nanoplastics showed significant memory and learning problems, along with neuron loss and reduced new brain cell growth in the hippocampus. The nanoplastics also disrupted gut bacteria and brain chemistry, with strong links found between gut microbiome changes and brain metabolic disruption, suggesting that plastic exposure during youth may impair brain development through the gut-brain connection.
Polystyrene micro/nanoplastics (MPs/NPs) are globally recognized environmental concerns due to their widespread pollution and detrimental effects on physiological functions. However, the neurotoxic effects and underlying mechanisms of MPs/NPs on brain function in adolescents remain incompletely understood. This study investigated the effects of polystyrene MPs/NPs on neurobehavioral function in adolescent mice, utilizing multi-omic analysis and molecular biology assays to explore potential mechanisms. Following oral exposure of MPs (5 μm) or NPs (0.5 μm) at 0.5 mg/day for 4 weeks, NPs induced more severe cognitive impairment in mice than MPs, as assessed by the Morris water maze and Y-maze tests. This impairment might be associated with the neuron loss and neurogenesis inhibition caused by NPs, while dendritic spine loss mediated by MPs in the hippocampus. Furthermore, analysis of hippocampal transcriptome and Western blotting indicated the potential involvement of the PI3K/AKT pathway in NPs-induced neurotoxicity. Meanwhile, exposure to NPs induced more pronounced disruptions in the hippocampal metabolome and gut microbiota, and strong correlations were observed between changes in hippocampal metabolites and gut bacteria. This study elucidated the toxicity mechanism of MPs and NPs in inducing cognitive impairment in adolescent mice, providing insights into their toxicological impacts and potential strategies for intervention.
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Researchers found that polystyrene nanoplastics given orally to mice crossed the blood-brain barrier and caused neuronal damage in the hippocampus, the brain region responsible for learning and memory. The nanoplastics disrupted the gut-brain connection by altering gut bacteria and circadian rhythm pathways, leading to measurable declines in learning and memory ability. This study provides a biological mechanism showing how ingested plastic nanoparticles could contribute to brain-related health problems in humans.
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Researchers found that mice exposed to polystyrene microplastics for eight weeks showed impaired learning and memory, with plastic particles detected in their hippocampus, the brain region critical for memory formation. The microplastics caused neuroinflammation, disrupted synaptic signaling, and altered gene expression in the brain. Interestingly, cutting the vagus nerve partially prevented these effects, suggesting that gut-brain communication plays a role in how ingested microplastics affect cognitive function.
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Mice that consumed polystyrene microplastics over an extended period showed reduced immune cells called macrophages in their colons and changes in gut bacteria that were linked to altered brain chemistry. This study provides evidence for a gut-brain connection where microplastics may affect brain function indirectly by first disrupting gut health and the immune system.
Intergenerational neurotoxicity of polystyrene nanoplastics in offspring mice is mediated by dysfunctional microbe-gut-brain axis
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Researchers found that mother mice exposed to polystyrene nanoplastics during pregnancy and nursing passed neurological harm to their offspring, with the babies showing brain inflammation, disrupted dopamine and serotonin signaling, and gut microbiome imbalances — suggesting that nanoplastic exposure before birth can damage the developing brain through the gut-brain connection.
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Researchers exposed mice to polystyrene nanoplastics during the perinatal period and found that the offspring developed depression-like behaviors, reduced social interactions, and diminished social dominance as adults. The nanoplastics caused structural damage to hippocampal neurons and disrupted gut microbiota composition, particularly in male offspring. The study suggests that early-life nanoplastic exposure may affect brain development and behavior through the microbiota-gut-brain axis.
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