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Polystyrene nanoplastics induce cognitive dysfunction and dendritic spine deterioration via excessive mitochondrial fission
Summary
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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