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20 resultsShowing papers similar to Polystyrene nanoplastics induced learning and memory impairments in mice by damaging the glymphatic system
ClearAdolescent 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.
Exposure to polystyrene microplastics impairs hippocampus-dependent learning and memory in mice
Researchers found that mice exposed to polystyrene microplastics for eight weeks showed impaired learning and memory, with plastic particles detected in their hippocampus, the brain region critical for memory formation. The microplastics caused neuroinflammation, disrupted synaptic signaling, and altered gene expression in the brain. Interestingly, cutting the vagus nerve partially prevented these effects, suggesting that gut-brain communication plays a role in how ingested microplastics affect cognitive function.
The gut-brain axis involved in polystyrene nanoplastics-induced neurotoxicity via reprogramming the circadian rhythm-related pathways
Researchers found that polystyrene nanoplastics given orally to mice crossed the blood-brain barrier and caused neuronal damage in the hippocampus, the brain region responsible for learning and memory. The nanoplastics disrupted the gut-brain connection by altering gut bacteria and circadian rhythm pathways, leading to measurable declines in learning and memory ability. This study provides a biological mechanism showing how ingested plastic nanoparticles could contribute to brain-related health problems in humans.
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 microplastics affect learning and memory in mice by inducing oxidative stress and decreasing the level of acetylcholine
Researchers exposed mice to polystyrene microplastics orally for four weeks and found that the particles impaired learning and memory functions. The microplastics caused oxidative stress in the brain and reduced levels of acetylcholine, a neurotransmitter critical for memory. The study suggests that microplastic ingestion may pose neurotoxic risks by disrupting brain chemistry and damaging nerve cells.
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.
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.
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.
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.
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.
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.
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.
Manifestation of polystyrene microplastic accumulation in brain with emphasis on morphometric and histopathological changes in limbic areas of Swiss albino mice
Mice exposed to polystyrene microplastics showed cognitive impairment, anxiety-like behavior, and measurable brain damage, particularly in the limbic system regions responsible for memory and emotion. The microplastics accumulated in the brain and caused neuron loss in the hippocampus, along with structural damage to the cortex, amygdala, and hypothalamus. This study provides direct evidence that microplastics can reach the brain and cause physical changes that affect behavior and mental function.
Exposure to Polystyrene Nanoplastics Led to Learning and Memory Deficits in Zebrafish by Inducing Oxidative Damage and Aggravating Brain Aging
Zebrafish exposed to polystyrene nanoplastics developed significant learning and memory problems, taking longer to navigate mazes and showing signs of accelerated brain aging. The nanoplastics caused oxidative damage, energy shortages, and disrupted the cell cycle in brain tissue. This study adds to growing evidence that nanoplastics small enough to cross the blood-brain barrier could impair cognitive function, raising concerns about long-term brain health effects from environmental nanoplastic exposure.
Pulmonary Flora‐Derived Lipopolysaccharide Mediates Lung‐Brain Axis through Activating Microglia Involved in Polystyrene Microplastic‐Induced Cognitive Dysfunction
In a mouse study, inhaling polystyrene microplastics impaired learning and memory -- even though the plastics never reached the brain directly. Instead, the microplastics changed the bacterial community in the lungs, which produced inflammatory signals that traveled to the brain and triggered damage, revealing a lung-to-brain pathway for microplastic harm.
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.
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.
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.
Primary astrocytes as a cellular depot of polystyrene nanoparticles
Researchers found that astrocytes — support cells in the brain — absorb polystyrene nanoplastics far more efficiently than neurons and act as a cellular buffer to protect nerve cells, but become overactivated when the particle load is too high, losing their protective function and potentially contributing to neurological harm.
Long-term exposure to polystyrene microplastics reduces macrophages and affects the microbiota–gut–brain axis in mice
Mice that consumed polystyrene microplastics over an extended period showed reduced immune cells called macrophages in their colons and changes in gut bacteria that were linked to altered brain chemistry. This study provides evidence for a gut-brain connection where microplastics may affect brain function indirectly by first disrupting gut health and the immune system.