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61,005 resultsShowing papers similar to Short-term PS-NP exposure in early adulthood induces neuronal damage in middle-aged mice via microglia-mediated neuroinflammation
ClearNeurotoxic 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.
Lifelong 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.
Adolescent exposure to micro/nanoplastics induces cognitive impairments in mice with neuronal morphological damage and multi-omic alterations
Adolescent mice exposed to polystyrene nanoplastics showed significant memory and learning problems, along with neuron loss and reduced new brain cell growth in the hippocampus. The nanoplastics also disrupted gut bacteria and brain chemistry, with strong links found between gut microbiome changes and brain metabolic disruption, suggesting that plastic exposure during youth may impair brain development through the gut-brain connection.
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.
Polystyrene nanoplastics penetrate across the blood-brain barrier and induce activation of microglia in the brain of mice
Researchers demonstrated that 50-nanometer polystyrene nanoplastics can cross the blood-brain barrier in mice, accumulate in brain tissue, and activate immune cells called microglia that then damage neurons. The nanoplastics disrupted the tight junctions that normally protect the brain, creating openings for the particles to pass through. This study provides direct evidence that nanoplastics can reach the brain and trigger inflammation, raising concerns about potential neurological effects of long-term nanoplastic exposure in humans.
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 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.
Food-borne polystyrene microplastic exposure exacerbates cognitive deficiency via enhanced neuronal synaptic damage and neuroinflammation in Alzheimer's disease
This study exposed Alzheimer's disease model mice (APP/PS1) to polystyrene microplastics via food and found that MP exposure worsened cognitive deficits by exacerbating hippocampal mitochondrial damage and neuroinflammation. The results suggest MP exposure may accelerate Alzheimer's disease progression in vulnerable individuals.
Inhalation of nanoplastics in the mouse model: Tissue bio-distribution and effects on the olfactory system
Mice that inhaled polystyrene nanoplastics for one week accumulated the particles in their brains, lungs, fat tissue, and testicles. Although the particles cleared from most tissues within a month, the mice suffered lasting damage to their sense of smell, with reduced brain cell function and signs of inflammation in the olfactory region. This is the first study to show that inhaled nanoplastics can impair the sense of smell and trigger long-term brain changes, even after the particles are gone.
Polystyrene nanoplastics induced learning and memory impairments in mice by damaging the glymphatic system
Mice exposed to polystyrene nanoplastics through different routes developed learning and memory problems linked to damage in their brain's waste-clearing system, called the glymphatic system. Amino-modified nanoplastics caused the most severe effects, disrupting the channels that normally flush toxins from the brain during sleep, suggesting a mechanism by which plastic pollution could contribute to cognitive decline.
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.
To what extent are orally ingested nanoplastics toxic to the hippocampus in young adult rats?
Researchers investigated polystyrene nanoplastic toxicity to the hippocampus in young adult rats, finding that oral exposure caused oxidative stress, inflammation, and histopathological changes in brain tissue with potential implications for cognitive function.
Identification of ceRNA network to explain the mechanism of cognitive dysfunctions induced by PS NPs in mice
Researchers exposed mice to polystyrene nanoplastics for six months and found dose-dependent cognitive decline along with increased oxidative stress and DNA damage in the prefrontal cortex. The study identified a competing endogenous RNA network involving circRNAs, miRNAs, and mRNAs that may explain the molecular mechanism behind nanoplastic-induced neurotoxicity.
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.
In vivo impact assessment of orally administered polystyrene nanoplastics: biodistribution, toxicity, and inflammatory response in mice
Researchers orally administered polystyrene nanoplastics to mice for two weeks and tracked their distribution and biological effects. The nanoplastics accumulated primarily in the intestine, kidneys, and liver, triggering significant inflammatory responses and oxidative stress in these organs despite no visible tissue damage. The study provides evidence that even short-term oral exposure to nanoplastics can cause meaningful inflammatory changes in multiple organ systems.
Effects of exposure to micro/nanoplastics of polystyrene on neuronal oxidative stress, neuroinflammation, and anxiety-like behavior in mice: A Systematic Review
This systematic review examined 24 studies on how polystyrene microplastics and nanoplastics affect the brains of mice. The findings consistently showed that exposure led to increased oxidative stress, brain inflammation, and anxiety-like behavior. Maternal exposure also caused brain-related harm in offspring, suggesting these tiny plastic particles could pose real risks to the nervous system.
Long-term polystyrene nanoparticles exposure reduces electroretinal responses and exacerbates retinal degeneration induced by light exposure
Researchers found that three months of polystyrene nanoplastic exposure in mice caused particles to penetrate the blood-retinal barrier, accumulate in retinal tissue, generate oxidative stress, and reduce light-sensitivity responses — and that prior nanoplastic exposure significantly worsened light-induced photoreceptor degeneration, with a transcriptomic profile resembling age-related macular degeneration.
Brain under siege: the role of micro and nanoplastics in neuroinflammation and oxidative stress
This review examines emerging evidence that micro- and nanoplastics can cross the blood-brain barrier and accumulate in nervous tissue, potentially triggering neuroinflammation and oxidative stress. Researchers summarized findings showing these particles may act as neurotoxicants that contribute to synaptic dysfunction and pathological changes in brain cells. The study highlights the need for further research into how chronic plastic particle exposure may affect central nervous system health over time.
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.
Neuronal damage induced by nanopolystyrene particles in nematodeCaenorhabditis elegans
C. elegans nematodes were chronically exposed to nanopolystyrene particles and found to develop neuronal damage affecting both development and function of the nervous system after long-term exposure at environmentally relevant concentrations. The study provides early evidence that nanoplastics can cause neurological harm in an animal model, raising questions about potential neurotoxicity in other species.
From exposure to neurotoxicity induced by micro-nanoplastics with brain accumulation and cognitive decline
This review synthesizes evidence that micro- and nanoplastics can reach the brain by crossing the blood-brain barrier or traveling along nerve pathways, accumulating in regions critical for memory and thinking. Animal studies show that chronic exposure leads to cognitive problems, behavioral changes, and brain changes resembling neurodegenerative diseases, driven by oxidative stress, inflammation, and disruption of the gut-brain connection. The findings raise concern that long-term human exposure to nanoplastics through food and air could contribute to cognitive decline and neurological disease.
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.
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.
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.