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61,005 resultsShowing papers similar to Early-life exposure to polystyrene nanoplastics at ambient doses induces neurotoxicity via mTOR-mediated autophagy-lysosomal dysfunction and proteostasis imbalance
ClearLifelong exposure to polystyrene-nanoplastics induces an attention-deficit hyperactivity disorder-like phenotype and impairs brain aging in mice
Mice exposed to nanoplastics throughout their entire lives -- from the womb through old age -- developed ADHD-like symptoms as adults, including hyperactivity, risk-taking behavior, and impaired learning, and showed a lower seizure threshold in old age. These behavioral changes were accompanied by altered brain proteins and accelerated brain aging at the cellular level, suggesting lifelong nanoplastic exposure may contribute to neurodevelopmental and neurodegenerative disorders.
Alleviation of neurotoxicity induced by polystyrene nanoplastics by increased exocytosis from neurons
Researchers investigated how polystyrene nanoplastics accumulate in neurons and cause toxic effects on brain cells. They found that inhibiting a specific protein involved in transporting particles within cells promoted the export of nanoplastics from neurons, reducing their harmful effects. The study suggests that enhancing the cell's natural ability to expel nanoplastics could be a potential strategy for alleviating their neurotoxic impact.
Perinatal exposure to polystyrene nanoplastics alters socioemotional behaviors via the microbiota–gut–brain axis in adult offspring mice
Researchers exposed mice to polystyrene nanoplastics during the perinatal period and found that the offspring developed depression-like behaviors, reduced social interactions, and diminished social dominance as adults. The nanoplastics caused structural damage to hippocampal neurons and disrupted gut microbiota composition, particularly in male offspring. The study suggests that early-life nanoplastic exposure may affect brain development and behavior through the microbiota-gut-brain axis.
Polystyrene nanoplastics exposure induces cognitive impairment in mice via induction of oxidative stress and ERK/MAPK-mediated neuronal cuproptosis
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.
Integrated transcriptomics and metabolomics reveal the mechanism of polystyrene nanoplastics toxicity to mice
Researchers used gene expression and metabolic profiling to understand how polystyrene nanoplastics harm mice at the molecular level, finding disrupted energy metabolism, fat processing, and amino acid pathways in the liver. These molecular changes suggest that nanoplastic exposure could contribute to metabolic disorders, with effects becoming more severe at higher doses.
Polystyrene nanoplastics induce cognitive dysfunction and dendritic spine deterioration via excessive mitochondrial fission
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.
Exposure to polystyrene nanoplastics induces an anxiolytic-like effect, changes in antipredator defensive response, and DNA damage in Swiss mice
Researchers exposed male Swiss mice to polystyrene nanoplastics at two doses over 20 days and assessed behavioral, neurological, and genetic effects. The study found that nanoplastic exposure induced anxiolytic-like behavior, altered antipredator defensive responses, and caused DNA damage in erythrocytes, suggesting that nanoplastics can affect mammalian brain function and genomic integrity.
Exposure to polystyrene nanoplastics causes anxiety and depressive-like behavior and down-regulates EAAT2 expression in mice
Mice exposed to polystyrene nanoplastics for two months developed anxiety and depression-like behaviors linked to reduced brain cell communication in the prefrontal cortex, caused by overactive support cells blocking a key brain chemical recycling system. When researchers activated the blocked recycling protein (EAAT2), the anxiety and depression symptoms were reversed, suggesting a potential treatment approach for nanoplastic-related mental health effects.
Short-term PS-NP exposure in early adulthood induces neuronal damage in middle-aged mice via microglia-mediated neuroinflammation
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.
Revealing the underlying mechanisms of nanoplastics induces neuroinflammation: From transcriptomic analysis to in vivo and in vitro validation
This study investigated how nanoplastics cause brain inflammation in mice. Researchers found that polystyrene nanoplastics accumulated in the brain, triggered anxiety-like behavior and cognitive problems, and activated inflammatory pathways involving NF-kappaB signaling. The evidence indicates that nanoplastics can cross into the brain and activate immune cells there, pointing to specific molecular mechanisms that may underlie the neurological effects of plastic particle exposure.
Neurotoxic effects of polystyrene nanoplastics on memory and microglial activation: Insights from in vivo and in vitro studies
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.
Cerebral to Systemic Representations of Alzheimer’s Pathogenesis Stimulated by Polystyrene Nanoplastics
Researchers found that environmentally realistic levels of polystyrene nanoplastics worsened Alzheimer's disease symptoms in mice, triggering brain inflammation, neuron death, and cognitive decline. The nanoplastics also disrupted metabolism and caused organ damage beyond the brain, including liver and kidney effects. This study provides some of the first evidence that nanoplastic exposure could accelerate brain diseases like Alzheimer's, especially as nanoplastics have been found in human brain tissue.
Polystyrene nanoplastics exposure caused defective neural tube morphogenesis through caveolae-mediated endocytosis and faulty apoptosis
This study found that polystyrene nanoplastics caused abnormal neural tube formation in early embryonic development by being taken up through a specific cellular pathway and triggering defective cell death. The findings suggest nanoplastics could potentially interfere with fetal brain development, raising serious concerns about exposure during pregnancy.
Cerebral to SystemicRepresentations of Alzheimer’sPathogenesis Stimulated by Polystyrene Nanoplastics
Researchers exposed both wild-type and APP/PS1 Alzheimer's model mice to environmental levels of polystyrene nanoplastics and measured Alzheimer's-like pathology progression. Nanoplastics exacerbated cognitive decline, microglial activation, and hippocampal neuronal death, particularly in the Alzheimer's model, with systemic inflammatory effects suggesting plastic particles may accelerate neurodegeneration.
Intergenerational neurotoxicity of polystyrene nanoplastics in offspring mice is mediated by dysfunctional microbe-gut-brain axis
Researchers found that mother mice exposed to polystyrene nanoplastics during pregnancy and nursing passed neurological harm to their offspring, with the babies showing brain inflammation, disrupted dopamine and serotonin signaling, and gut microbiome imbalances — suggesting that nanoplastic exposure before birth can damage the developing brain through the gut-brain connection.
Neurotoxic potential of polystyrene nanoplastics in primary cells originating from mouse brain
Researchers exposed three types of primary mouse brain cells to 100 nm polystyrene nanoplastics and found that neurons underwent apoptosis while astrocytes survived but developed reactive astrocytosis with elevated inflammatory markers, suggesting that neuronal vulnerability to nanoplastic accumulation may be amplified by astrocyte-driven neuroinflammation.
Polystyrene micro- and nanoparticles exposure induced anxiety-like behaviors, gut microbiota dysbiosis and metabolism disorder in adult mice
A mouse study found that exposure to both micro- and nano-sized polystyrene particles caused anxiety-like behavior, disrupted gut bacteria, and altered metabolism. The nanoplastics caused more severe effects than the larger microplastics, and longer exposure periods made the damage worse. These findings support the idea that plastic particles can affect brain function and behavior through the gut-brain connection.
Manifestation of polystyrene microplastic accumulation in tissues of vital organs including brain with histological and behaviour analysis on Swiss albino mice
Researchers exposed rats to polystyrene microplastics and examined accumulation in vital organs including the brain, liver, kidney, and gut, finding tissue-specific deposition that was associated with behavioral changes and organ-level pathological effects.
Neonatal Exposure to Polystyrene Nanoplastics Impairs Microglia-Mediated Synaptic Pruning and Causes Social Behavioral Defects in Adulthood
Newborn mice exposed to polystyrene nanoplastics showed disrupted brain development that led to social behavior problems lasting into adulthood. The nanoplastics impaired microglia -- the brain's immune cells -- preventing them from properly pruning unnecessary connections between nerve cells during a critical window of early development. This raises concerns about nanoplastic exposure from baby bottles and other infant products.
Maternal exposure to polystyrene nanoplastics impacts developmental milestones and brain structure in mouse offspring
Researchers exposed pregnant mice to polystyrene nanoplastics and studied the effects on their offspring's brain development. The study found that maternal nanoplastic exposure affected developmental milestones and brain structure in the young mice. The findings suggest that nanoplastic exposure during pregnancy may pose risks to fetal brain development, though more research is needed to understand the implications for humans.
Polystyrene microplastics disrupt osteogenic differentiation via lysosome-mediated mitochondrial dysfunction: Protective role of mTOR signaling
Researchers identified a mechanistic pathway by which polystyrene microplastics impair bone formation in zebrafish and mouse preosteoblasts: PS-MPs accumulate in lysosomes, trigger mitochondrial dysfunction, and suppress osteogenic differentiation. Activation of the mTOR signaling pathway was found to partially protect against this bone toxicity.
Teratological, neurochemical and histomorphic changes in the limbic areas of F1 mice progeny due to co-parental polystyrene nanoplastic exposure
Researchers exposed parent mice to polystyrene nanoplastics before and during pregnancy and found that offspring exhibited skeletal and visceral malformations, impaired neonatal reflexes, learning deficits, and structural brain changes — including reduced hippocampal neurons — demonstrating transgenerational neurodevelopmental harm from nanoplastic exposure.
A new mechanism for ubiquitination in polystyrene nanoplastic-induced spatial cognitive dysfunction through microglial activation-induced apoptosis of neurons
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.
Lipid metabolic dysregulation: A novel developmental toxicity pathway of aged nanoplastics via inhibition of lipophagy in zebrafish
Researchers showed that UV-aged polystyrene nanoplastics cause more severe developmental toxicity in zebrafish larvae than pristine particles by blocking lipophagy — the cellular process of breaking down stored fat via lysosomes — leading to abnormal lipid accumulation and disrupted early development.