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Polystyrene nanoplastics exposure induces cognitive impairment in mice via induction of oxidative stress and ERK/MAPK-mediated neuronal cuproptosis
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This mouse study found that polystyrene nanoplastics caused cognitive impairment by triggering oxidative stress and activating a cell-death process called cuproptosis in brain neurons. The findings suggest that copper buildup and specific signaling pathways may be therapeutic targets for reducing brain damage from nanoplastic exposure, though these results still need to be confirmed in human-relevant models.
This study presents preliminary evidence indicating that PS-NPs may induce neuronal cuproptosis, potentially through the oxidative stress-mediated activation of the ERK-MAPK pathway, which contributes to cognitive dysfunction in mice. These findings provide insights into the potential mechanisms underlying PS-NPs neurotoxicity and highlight possible therapeutic targets, such as copper chelation or MAPK inhibition, for mitigating the neurological risks associated with nanoplastic exposure, pending further validation in human-relevant models.
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Polystyrene nanoplastics induce hippocampal damage and cognitive deficits through oxidative stress-triggered microglial extracellular traps and neuronal ferroptosis
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Researchers showed that polystyrene nanoplastics impair spatial memory in mice by triggering a cascade in which hippocampal oxidative stress activates microglia to release extracellular traps, sustaining neuroinflammation that drives neuronal ferroptosis — a form of iron-dependent cell death — and that the antioxidant N-acetylcysteine blocks this entire pathway and preserves cognitive function.
Murine hippocampal CA3 vulnerability to intravenously administered polystyrene nanoplastics: preferential accumulation and ROS-related neuronal cell death
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In mice injected with tiny polystyrene plastic particles, the particles built up mainly in a specific brain region (hippocampal CA3), where nerve cells died off and showed signs of oxidative stress. These mice also performed worse on memory and learning tests compared to untreated mice.
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.
Coexposure to heat stress and polystyrene nanoplastics induces neuroinflammation and cognitive impairment via oxidative stress-NLRP6-pyroptosis axis
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Researchers exposed mice simultaneously to elevated heat (simulating climate warming) and polystyrene nanoplastics for 30 days, finding that combined exposure caused greater cognitive deficits, hippocampal neurodegeneration, and blood-brain barrier damage than either stressor alone — mediated by a novel NLRP6 inflammasome-pyroptosis pathway that antioxidant treatment could partially reverse.
Short-term PS-NP exposure in early adulthood induces neuronal damage in middle-aged mice via microglia-mediated neuroinflammation
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Researchers orally dosed young mice with polystyrene nanoplastics for one week and observed, ten months later, that particles persisted in brain tissue and drove microglial-mediated neuroinflammation, synapse loss, and cognitive impairment — with minocycline treatment confirming that microglial activation was the key driver of long-term neuronal damage.
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