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20 resultsShowing papers similar to Polystyrene Microplastics Disrupt the Gut-Brain Axis via Activating Brain TLR4 and Impair Hippocampal Synapses through the TLR4/MyD88/NF-κB Pathway
ClearThe 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.
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.
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.
Nanoplastics activate a TLR4/p38-mediated pro-inflammatory response in human intestinal and mouse microglia cells
Researchers exposed human intestinal cells and mouse brain immune cells to polystyrene nanoplastics and found that the particles activated inflammatory pathways through a specific receptor called TLR4. The nanoplastics increased production of the inflammatory signal IL-1 beta in gut cells and triggered inflammation-promoting enzymes in brain immune cells. This study provides a mechanism by which nanoplastics swallowed in food or water could trigger inflammation in both the gut and the brain.
Association between long-term exposure of polystyrene microplastics and exacerbation of seizure symptoms: Evidence from multiple approaches
This study found that long-term exposure to polystyrene microplastics may worsen seizure symptoms by disrupting gut bacteria and triggering inflammation that damages brain cells. Using both human data and animal experiments, the researchers showed that microplastics can set off a chain reaction from the gut to the brain, leading to a type of cell death called ferroptosis in the hippocampus. The findings suggest that chronic microplastic exposure could be a hidden risk factor for people with seizure disorders.
Polystyrene microplastics trigger colonic inflammation in rats via the TLR4/NF-κB/COX-2 pathway and modulation of intestinal microbiota
Rats exposed to polystyrene microplastics for 90 days developed significant colon inflammation, including damaged gut lining, increased inflammatory markers, and disrupted gut bacteria. The study identified a specific inflammatory pathway (TLR4/NF-kB/COX-2) through which microplastics trigger intestinal inflammation, providing important clues about how plastic particles in food and water could contribute to gut diseases in humans.
Innovative mechanisms of micro- and nanoplastic-induced brain injury: Emphasis on the microbiota-gut-brain axis
This review summarizes how micro- and nanoplastics may damage the brain through the gut-brain axis, a communication pathway between the digestive system and the nervous system. Nanoplastics can disrupt gut bacteria and weaken the intestinal barrier, potentially sending inflammatory signals to the brain. The authors suggest that targeting gut health could be a way to reduce brain damage caused by nanoplastic exposure.
Microbiota-mediated metabolic perturbations in the gut and brain of mice after microplastic exposure
In a mouse study, oral exposure to polystyrene microplastics of two sizes altered the gut bacteria community and caused metabolic changes in both the intestines and the brain. The disrupted gut bacteria appeared to drive changes in bile acid, energy, and other metabolic pathways. These findings support the idea that microplastics in food and water could affect brain health indirectly by first disrupting the gut microbiome and its chemical signals.
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.
Microplastics and the gut-brain axis: Unraveling neurotoxic mechanisms and health implications
This review examines how microplastics interact with the gut-brain axis, a communication network linking the digestive system to the central nervous system. Researchers found that microplastics can disrupt intestinal barrier integrity, alter gut microbiota composition, and trigger systemic inflammation that may affect neurotransmitter balance and brain function. The study suggests that chronic microplastic exposure through the diet could contribute to neurological effects through inflammatory and oxidative stress pathways.
Deciphering the Neurotoxic Burden of Micro- and Nanoplastics: From Multi-model Experimental Evidence to Therapeutic Innovation
This review summarizes research on how micro- and nanoplastics damage the brain and nervous system, covering evidence from cell studies, animal experiments, and clinical observations. Plastic particles can cross the blood-brain barrier, disrupt the gut-brain connection, cause oxidative stress, and trigger inflammation that leads to memory problems and cognitive decline. The review also discusses potential treatment strategies, making it a useful resource for understanding the brain health risks of plastic exposure.
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.
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.
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.
Polystyrene Nanoplastics Toxicity to Zebrafish: Dysregulation of the Brain–Intestine–Microbiota Axis
This study found that polystyrene nanoplastics disrupted the brain-gut connection in zebrafish at environmentally realistic concentrations, affecting growth, gut health, and brain chemistry. The nanoplastics altered neurotransmitter levels, particularly reducing a dopamine-related compound, and changed the balance of gut bacteria in ways that correlated with brain changes. These findings suggest a pathway by which nanoplastics in food and water could affect both digestive and brain health through the gut-brain axis.
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.
Oral exposure of polystyrene microplastics and doxycycline affects mice neurological function via gut microbiota disruption: The orchestrating role of fecal microbiota transplantation
Mice exposed to both polystyrene microplastics and the antibiotic doxycycline showed brain inflammation and declines in learning and memory, driven by disruptions to their gut bacteria. Fecal transplants from healthy mice reversed some of these brain effects, confirming the gut-brain connection plays a key role. This suggests that microplastics combined with common antibiotics could harm brain function through changes in the gut microbiome.
Nanoplastic Impact on the Gut-Brain Axis: Current Knowledge and Future Directions
Researchers reviewed the emerging evidence on how nanoplastics may affect the gut-brain axis, the communication pathway between the digestive and nervous systems. Studies indicate that nanoplastic exposure can alter gut microbiota, increase intestinal permeability, trigger oxidative stress and inflammation, and produce neurotoxic and behavioral effects. The review calls for more research given the ubiquitous presence of plastics in the human environment and the potential for nanoplastics to disrupt this critical biological communication pathway.
Exposure to polystyrene microplastics reduces sociality and brain oxytocin levels through the gut-brain axis in mice
Adolescent mice exposed to polystyrene microplastics for 10 weeks showed reduced social behavior and lower levels of oxytocin -- a hormone important for social bonding -- in a key brain region. The microplastics damaged the gut lining and altered gut bacteria, and when researchers blocked the nerve connection between the gut and brain, the social behavior problems improved. This provides strong evidence that microplastics can affect brain function and social behavior through the gut-brain axis.
Dysregulation of the microbiota-brain axis during long-term exposure to polystyrene nanoplastics in rats and the protective role of dihydrocaffeic acid
Researchers exposed rats to low doses of polystyrene nanoplastics over 24 weeks and observed disruptions in the gut-brain connection, including changes in gut bacteria, intestinal damage, and altered brain function. A natural compound called dihydrocaffeic acid showed protective effects against these nanoplastic-induced harms. The study suggests that long-term nanoplastic exposure may disrupt the communication between gut microbes and the brain, with potential implications for neurological health.