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20 resultsShowing papers similar to Polystyrene nanoplastics induce cognitive dysfunction and dendritic spine deterioration via excessive mitochondrial fission
ClearPolystyrene nanoplastics target electron transport chain complexes in brain mitochondria
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.
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.
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.
Exposure to different surface-modified polystyrene nanoparticles caused anxiety, depression, and social deficit in mice via damaging mitochondria in neurons
Mice exposed to polystyrene nanoplastics with different surface coatings all developed anxiety, depression, and impaired social behavior after the particles accumulated in their brains. The nanoplastics crossed the blood-brain barrier by disrupting the connections between blood vessel cells, then damaged the mitochondria (energy producers) inside brain neurons, reducing their energy output and likely driving the behavioral changes.
Cationic nanoplastic causes mitochondrial dysfunction in neural progenitor cells and impairs hippocampal neurogenesis
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.
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.
Mechanisms of micro- and nanoplastics on blood-brain barrier crossing and neurotoxicity: Current evidence and future perspectives
This review examines evidence that micro- and nanoplastics can cross the blood-brain barrier, the protective shield around the brain, through multiple pathways including disrupting the barrier's tight junctions and being transported inside cells. Once in the brain, these particles may cause damage through oxidative stress, inflammation, mitochondrial dysfunction, and disrupted iron metabolism, with effects worsened when plastics carry other pollutants like heavy metals.
Crossing barriers – tracking micro- and nanoplastic pathways into the human brain
Researchers tracked potential pathways by which micro- and nanoplastics may enter the human brain, examining both in vitro cell models and post-mortem brain tissue. They found that human monocytes rapidly internalized polystyrene particles into endocytic vesicles and mitochondria, and detected plastic particles in brain tissue samples, providing evidence that nanoplastics may be capable of crossing brain barriers.
Environmental nanoplastics induce mitochondrial dysfunction: A review of cellular mechanisms and associated diseases
This review summarizes how nanoplastics, which are small enough to enter individual cells, damage mitochondria (the energy-producing structures inside cells) by disrupting their shape, function, and ability to produce energy. This mitochondrial damage has been linked to a range of diseases including neurodegeneration, diabetes, cardiovascular disease, and reproductive problems. The findings help explain why nanoplastic exposure may contribute to multiple chronic health conditions through a common cellular mechanism.
Nanoplastics exposure-induced mitochondrial dysfunction contributes to disrupted stem cell differentiation in human cerebral organoids
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.
Inhibiting ferroptosis in brain microvascular endothelial cells: A potential strategy to mitigate polystyrene nanoplastics‒induced blood‒brain barrier dysfunction
Researchers found that polystyrene nanoplastics disrupt the blood-brain barrier in mice by triggering ferroptosis — an iron-dependent form of cell death — in brain microvascular endothelial cells, and that blocking ferroptosis with a targeted drug reduced tight junction protein loss and restored barrier integrity.
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.
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.
Polystyrene nanoplastics promote the blood-brain barrier dysfunction through autophagy pathway and excessive erythrophagocytosis
Polystyrene nanoplastics (extremely tiny plastic particles) were found to damage the blood-brain barrier, the protective shield that keeps harmful substances out of the brain. The particles disrupted brain cell function by interfering with iron regulation and also damaged red blood cells, which then caused further harm to the barrier, revealing multiple ways that nanoplastics could threaten brain health.
Assessing micro and nanoplastics toxicity using rodent models: Investigating potential mitochondrial implications
This review examines recent rodent studies investigating how micro- and nanoplastics affect cellular health, with a focus on potential mitochondrial impacts. Researchers found that while no study has directly targeted mitochondrial effects, several reported molecular and biochemical changes consistent with disrupted mitochondrial function, including oxidative stress. The study suggests that mitochondria may be an important but understudied target of micro- and nanoplastic toxicity.
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.
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.
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.
Early-life exposure to polystyrene nanoplastics at ambient doses induces neurotoxicity via mTOR-mediated autophagy-lysosomal dysfunction and proteostasis imbalance
Researchers exposed young mice to environmentally relevant doses of polystyrene nanoplastics and found that the particles penetrated their brains and caused behavioral and emotional disorders. The study identified a specific molecular mechanism in which nanoplastics disrupted the mTOR signaling pathway, leading to lysosomal dysfunction and a buildup of misfolded proteins that ultimately caused neurotoxicity. Treatments targeting these pathways were able to alleviate the harmful effects, suggesting potential avenues for intervention.
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.