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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.
Our research addresses the critical issue of polystyrene nanoplastics (PS-NPs) exposure and their neurotoxic effects, highlighting a significant environmental health concern. We proved that PS-NPs could breach the blood-brain barrier (BBB) and accumulate in murine brains, emphasizing the need for further investigation into their impact on human health. Using both in vivo models with Thy1-GFP-M transgenic mice and in vitro models with primary hippocampal neurons, we explored the effects of PS-NPs on cognitive function and neuroplasticity. Our results revealed that PS-NPs lead to cognitive impairment, evidenced by impaired performance in behavioral tests. Additionally, PS-NPs caused a significant reduction in dendritic spine density and altered the morphology of spines in hippocampal CA1 neurons. We explored the underlying mechanisms, finding that PS-NPs induced mitochondrial dysfunction, characterized by decreased membrane potential, reduced ATP production, and excessive mitochondrial fission. This mitochondrial disruption was associated with excessive mitophagy. Importantly, Mitochondrial Division Inhibitor-1 (Mdivi-1) treatment alleviated the neurotoxic effect, stabilized mitochondrial function, maintained dendritic spine density, and reversed the cognitive impairment induced by the PS-NPs. Overall, our study highlights the significant neurotoxic potential of PS-NPs and suggests that targeting mitochondrial fission can be a viable therapeutic strategy. This work underscores the urgent need to understand the neurological consequences of NPs exposure and develop strategies to counteract their health risks.
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Researchers investigated the effects of polystyrene nanoplastics on mitochondrial function in rat brain tissue. They found that nanoplastic exposure significantly impaired the electron transport chain, specifically disrupting electron flow between respiratory complexes I-III and II-III in both synaptic and non-synaptic mitochondria. The findings reveal a potential mechanism by which nanoplastics could contribute to brain energy metabolism deficits and neurotoxicity.
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.
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Researchers found that polystyrene nanoparticles disrupt microglial lipid metabolism in the brain by suppressing the protein RNF139, which leads to SREBP activation, mitochondrial dysfunction, and inflammatory signaling that ultimately kills neurons and impairs spatial memory in mice.
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.
Exposure to different surface-modified polystyrene nanoparticles caused anxiety, depression, and social deficit in mice via damaging mitochondria in neurons
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Mice exposed to polystyrene nanoplastics with different surface coatings all developed anxiety, depression, and impaired social behavior after the particles accumulated in their brains. The nanoplastics crossed the blood-brain barrier by disrupting the connections between blood vessel cells, then damaged the mitochondria (energy producers) inside brain neurons, reducing their energy output and likely driving the behavioral changes.
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