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61,005 resultsShowing papers similar to Exposure to Polystyrene Microplastics Promotes the Progression of Cognitive Impairment in Alzheimer’s Disease: Association with Induction of Microglial Pyroptosis
ClearFood-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.
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.
Short-Term Exposure to Polystyrene Microplastics Alters Cognition, Immune, and Metabolic Markers in an APOE Genotype and Sex-Dependent Manner
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.
Microglial phagocytosis of polystyrene microplastics results in immune alteration and apoptosis in vitro and in vivo
Researchers found that polystyrene microplastics can cross the blood-brain barrier in mice after oral exposure and accumulate in brain tissue, where they are engulfed by microglia, the brain's immune cells. This engulfment triggered inflammatory responses and cell death in the microglia both in cell cultures and in living mice. The study suggests that microplastic exposure may affect brain immune function, with potential implications for neurological health.
Nanoplastics exposure exacerbates Aβ plaque deposition in Alzheimer’s disease mice by inducing microglia pyroptosis
In Alzheimer's disease model mice, exposure to environmentally relevant doses of nanoplastics worsened cognitive problems and increased the brain plaques associated with the disease. The nanoplastics damaged a waste-clearing system in brain immune cells called microglia, reducing their ability to remove harmful amyloid plaques, though the study also found that melatonin treatment helped restore brain cell function and reduce plaque buildup.
Co-exposure of polystyrene microplastics and iron aggravates cognitive decline in aging mice via ferroptosis induction
Researchers studied the combined effects of microplastic and iron exposure on cognitive function in aging mice. They found that polystyrene microplastics accumulated in the brain's cortex and hippocampus, and when combined with iron, significantly worsened cognitive decline through a cell death process called ferroptosis. The study suggests that co-exposure to microplastics and metals may pose heightened risks to brain health in aging populations.
Microglial clearance of Alzheimer's amyloid-beta obstructed by nanoplastics
Researchers found that polystyrene nanoplastics interfere with the brain's ability to clear amyloid-beta, the protein that builds up in Alzheimer's disease. The nanoplastics accelerated amyloid clumping and drained the energy of brain immune cells that normally clean up these harmful proteins. This study suggests that nanoplastic exposure could worsen or contribute to the development of Alzheimer's disease.
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 microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
Effects of Microplastic Accumulation on Neuronal Death After Global Cerebral Ischemia
Researchers found that microplastics worsened brain damage after a stroke-like event in mice, increasing inflammation, damaging the protective coating around nerve fibers, and causing more brain cell death. The microplastics also triggered the release of abnormal tau proteins, similar to what happens in Alzheimer's disease, suggesting that microplastic exposure could make the brain more vulnerable to injury and neurodegenerative conditions.
Microplastic Exposure Promotes Amyloid Misfolding and Metabolic Impairment at Sub-Lethal Doses in an In Vitro Cellular Model of Alzheimer’s Disease
Researchers exposed cellular models of Alzheimer's disease to sub-lethal polystyrene microplastics and nanoplastics and monitored amyloid protein misfolding and metabolic impairment using photothermal microscopy. Even low-dose plastic exposure promoted amyloid aggregation and disrupted cellular energy metabolism, suggesting microplastics may accelerate the molecular processes underlying Alzheimer's pathology.
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.
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.
Co-exposure to ozone and polystyrene nanoplastic exacerbates cognitive impairment and anxiety-like behavior by regulating neuronal pyroptosis in mice
Mice exposed to both ozone and polystyrene nanoplastics showed worse cognitive problems and anxiety-like behavior than those exposed to either pollutant alone. The combined exposure triggered a type of inflammatory cell death called pyroptosis in the brain's prefrontal cortex. This is concerning because people in polluted urban areas are routinely exposed to both ozone and airborne nanoplastics, and the combination may be more harmful to brain health than either one individually.
Polystyrene Micro- and Nanoplastic Exposure Triggers an Activation and Stress Response in Human Astrocytes
Researchers exposed primary human astrocytes to polystyrene micro- and nanoplastics and found that these particles triggered cellular stress responses, including increased production of reactive oxygen species and activation of inflammatory pathways. Nanoplastics were particularly effective at penetrating cells and disrupting normal astrocyte function. The findings suggest that plastic particle exposure may contribute to neuroinflammatory processes in the brain, warranting further investigation into potential neurotoxic effects.
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.
Evaluation of Neurotoxicity in BALB/c Mice following Chronic Exposure to Polystyrene Microplastics
Researchers found that chronic exposure to polystyrene microplastics in mice led to learning and memory problems along with signs of neurotoxicity. The study suggests that long-term microplastic exposure may impair brain function in mammals. These findings raise important questions about the potential neurological risks of microplastic exposure for the broader public.
Polystyrene Nano- and Microplastic Particles Induce an Inflammatory Gene Expression Profile in Rat Neural Stem Cell-Derived Astrocytes In Vitro
Researchers exposed brain cells derived from rat neural stem cells to polystyrene nano- and microplastics and found that astrocytes -- the most abundant brain support cells -- were the most affected, showing reduced survival and widespread changes in gene activity. The activated genes were involved in brain inflammation and immune responses, while genes for fat metabolism were turned down. These findings suggest that plastic particles reaching the brain could trigger inflammation that may contribute to neurological problems.
Association of microplastics in human cerebrospinal fluid with Alzheimer’s disease-related changes
Researchers detected four types of microplastics in human cerebrospinal fluid (the liquid surrounding the brain and spinal cord) and found that people with Alzheimer's disease markers had significantly higher levels of polyethylene and PVC. Higher microplastic levels in cerebrospinal fluid were linked to worse cognitive test scores and faster mental decline over one year, suggesting a potential connection between brain microplastic exposure and Alzheimer's progression.
Secondary brain injury after polystyrene microplastic-induced intracerebral hemorrhage is associated with inflammation and pyroptosis
Researchers studied how polystyrene microplastics affect brain tissue in chickens after six weeks of continuous exposure. The study found that microplastic exposure caused cerebral hemorrhage, microthrombi formation, and loss of Purkinje cells, with secondary brain injury driven by inflammatory responses and pyroptosis activation.
Microplastics induced apoptosis in macrophages by promoting ROS generation and altering metabolic profiles
This study found that polystyrene microplastics trigger cell death in macrophages, key immune cells that serve as the body's first line of defense against harmful substances. Smaller microplastics (0.5 micrometers) were more damaging than larger ones because they can enter the cells directly, where they generate harmful reactive oxygen species and disrupt normal cell metabolism.
Impact of nanoplastics on Alzheimer ’s disease: Enhanced amyloid-β peptide aggregation and augmented neurotoxicity
Researchers found that even very low concentrations of polystyrene nanoplastics can speed up the clumping of amyloid-beta protein, a hallmark of Alzheimer's disease, and increase its toxicity to brain cells. The hydrophobic (water-repelling) surface of the nanoplastics helps the proteins stick together faster, suggesting a potential link between environmental nanoplastic exposure and increased risk of Alzheimer's disease.
Pollutant-induced pyroptosis in humans and other animals
This review examines how environmental pollutants including particulate matter, cadmium, and polystyrene microplastics trigger pyroptosis, a pro-inflammatory form of cell death, across diverse tissues in mammals and birds.
The role of pyroptosis in inflammatory diseases
This review explains pyroptosis, a type of programmed cell death that triggers strong inflammation, and its role in diseases like infections, autoimmune conditions, and organ damage. While not focused on microplastics specifically, pyroptosis is one of the key mechanisms through which microplastic exposure may cause inflammation in tissues. Understanding this process helps explain how tiny plastic particles could trigger harmful immune responses in the body.