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Targeted activation of ErbB4 receptor ameliorates neuronal deficits and neuroinflammation in a food-borne polystyrene microplastic exposed mouse model
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In mice exposed to polystyrene microplastics through food, researchers found significant brain inflammation and cognitive problems, but activating a specific brain receptor (ErbB4) with a small molecule drug helped reverse these effects. This suggests that microplastic exposure through diet may contribute to brain damage, and points toward possible treatments for microplastic-related neurological harm.
The impact of polystyrene microplastics (PS-MPs) on the nervous system has been documented in the literature. Numerous studies have demonstrated that the activation of the epidermal growth factor receptor 4 (ErbB4) is crucial in neuronal injury and regeneration processes. This study investigated the role of targeted activation of ErbB4 receptor through a small molecule agonist, 4-bromo-1-hydroxy-2-naphthoic acid (C11H7BrO3, E4A), in mitigating PS-MPs-induced neuronal injury. The findings revealed that targeted activation of ErbB4 receptor significantly ameliorated cognitive behavioral deficits in mice exposed to PS-MPs. Furthermore, E4A treatment upregulated the expression of dedicator of cytokinesis 3 (DOCK3) and Sirtuin 3 (SIRT3) and mitigated mitochondrial and synaptic dysfunction within the hippocampus of PS-MPs-exposed mice. E4A also diminished the activation of the TLR4-NF-κB-NLRP3 signaling pathway, consequently reducing neuroinflammation. In vitro experiments demonstrated that E4A partially alleviated PS-MPs-induced hippocampal neuronal injury and its effects on microglial inflammation. In conclusion, the findings of this study indicate that targeted activation of ErbB4 receptor may mitigate neuronal damage and subsequent neuroinflammation, thereby alleviating hippocampal neuronal injury induced by PS-MPs exposure and ameliorating cognitive dysfunction. These results offer valuable insights for the development of potential therapeutic strategies.
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Researchers exposed human intestinal cells and mouse brain immune cells to polystyrene nanoplastics and found that the particles activated inflammatory pathways through a specific receptor called TLR4. The nanoplastics increased production of the inflammatory signal IL-1 beta in gut cells and triggered inflammation-promoting enzymes in brain immune cells. This study provides a mechanism by which nanoplastics swallowed in food or water could trigger inflammation in both the gut and the brain.
Neurotoxic effects of polystyrene nanoplastics on memory and microglial activation: Insights from in vivo and in vitro studies
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In a mouse study, tiny nanoplastics (30-50 nanometers) that were swallowed reached the brain and caused memory problems by activating the brain's immune cells, called microglia, which triggered inflammation. This is concerning because it shows that nanoplastics small enough to be found in everyday products like cosmetics could cross into the brain and impair cognitive function.
Polystyrene Microplastics Disrupt the Gut-Brain Axis via Activating Brain TLR4 and Impair Hippocampal Synapses through the TLR4/MyD88/NF-κB Pathway
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Scientists found that tiny plastic particles from polystyrene (commonly used in food containers and packaging) can damage the connection between your gut and brain when consumed. These microplastics disrupt healthy gut bacteria, allowing harmful substances to enter the bloodstream and eventually reach the brain, where they cause inflammation and damage to areas important for memory and learning. This research suggests that exposure to these tiny plastic particles could potentially contribute to brain health problems over time.
Promising protective potential of MiR-103a-3p against polystyrene microplastic neurotoxicity in rats
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Researchers discovered that a small molecule called miR-103a-3p can protect rat brains from the damage caused by polystyrene microplastics. When injected into the brain, miR-103a-3p reversed the learning and memory problems caused by microplastic exposure by reducing inflammation, oxidative stress, and cell death in the hippocampus. This finding points toward potential therapeutic strategies for counteracting the brain-damaging effects of microplastic exposure.
Short-Term Exposure to Polystyrene Microplastics Alters Cognition, Immune, and Metabolic Markers in an APOE Genotype and Sex-Dependent Manner
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Researchers exposed Alzheimer's disease mouse models to polystyrene microplastics for a short term and observed worsened cognitive performance, altered immune markers, and disrupted metabolic pathways, suggesting that MP exposure may accelerate neurological decline in individuals already vulnerable to dementia.
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