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Cationic nanoplastic causes mitochondrial dysfunction in neural progenitor cells and impairs hippocampal neurogenesis
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This study found that positively charged nanoplastics accumulated in the mitochondria of brain stem cells, causing energy depletion and stopping cell growth. In mice, 10 days of exposure impaired the formation of new brain cells in the hippocampus, a region critical for memory, and reduced memory retention. The findings suggest that nanoplastic exposure could deplete the brain's supply of stem cells, potentially contributing to cognitive decline and neurodegenerative conditions.
Nanoplastics (NPs) exposure to humans can occur through various routes, including the food chain, drinking water, skin contact, and respiration. NPs are plastics with a diameter of less than 100 nm and have the potential to accumulate in tissues, leading to toxic effects. This study aimed to investigate the neurotoxicity of polystyrene NPs on neural progenitor cells (NPCs) and hippocampal neurogenesis in a rodent model. Toxicity screening of polystyrene NPs based on their charge revealed that cationic amine-modified polystyrene (PS-NH) exhibited cytotoxicity, while anionic carboxylate-modified polystyrene (PS-COO) and neutral NPs (PS) did not. NPCs treated with PS-NH showed a significant reduction in growth rate due to G1 cell cycle arrest. PS-NH increased the expression of cell cycle arrest markers p21 and p27, while decreasing cyclin D expression in NPCs. Interestingly, PS-NH accumulated in mitochondria, leading to mitochondrial dysfunction and energy depletion, which caused G1 cell cycle arrest. Prolonged exposure to PS-NH in C17.2 NPCs increased the expression of p16 and senescence-associated secretory phenotype factors, indicating cellular senescence. In vivo studies using C57BL/6 mice demonstrated impaired hippocampal neurogenesis and memory retention after 10 days of PS-NH administration. This study suggests that NPs could deplete neural stem cell pools in the brain by mitochondrial dysfunction, thereby adversely affecting hippocampal neurogenesis and neurocognitive functions.
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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.
Nanoplastics exposure-induced mitochondrial dysfunction contributes to disrupted stem cell differentiation in human cerebral organoids
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Using lab-grown human brain organoids (miniature brain models), researchers found that polystyrene nanoplastics damaged mitochondria (the energy-producing structures in cells), leading to increased cell death and disrupted development of brain stem cells. These findings suggest that nanoplastic exposure could interfere with how brain cells develop and function, raising concerns about the neurological effects of environmental plastic pollution on humans.
Nanoplastics-induced neurotoxicity: neurovascular dysfunction, cognitive impairment, and mechanisms of cell death.
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This review summarizes existing research on how tiny plastic particles called nanoplastics may affect the brain. Studies in lab models suggest these particles can disrupt the brain's protective barrier, trigger cell stress and death, and interfere with brain cell communication, which researchers link to memory and behavior problems in experimental models.
Cytotoxicity of amine-modified polystyrene MPs and NPs on neural stem cells cultured from mouse subventricular zone
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Researchers tested the effects of polystyrene microplastics and nanoplastics with a positive surface charge on neural stem cells from mouse brains. Both sizes of particles reduced cell survival, but nanoplastics were significantly more toxic at lower concentrations, causing cell death and preventing stem cells from developing into mature brain cells. These findings suggest that nanoplastics that reach the brain could potentially harm the nervous system's ability to repair and maintain itself.
Polystyrene nanoplastics target electron transport chain complexes in brain mitochondria
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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.
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