We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Coexposure to heat stress and polystyrene nanoplastics induces neuroinflammation and cognitive impairment via oxidative stress-NLRP6-pyroptosis axis
AI summary Read the abstract
Researchers exposed mice simultaneously to elevated heat (simulating climate warming) and polystyrene nanoplastics for 30 days, finding that combined exposure caused greater cognitive deficits, hippocampal neurodegeneration, and blood-brain barrier damage than either stressor alone — mediated by a novel NLRP6 inflammasome-pyroptosis pathway that antioxidant treatment could partially reverse.
Global warming and plastic pollution constitute interconnected environmental threats. However, their combined neurotoxic effects, particularly in the context of climate change-driven temperature rise, remain unexplored, posing a critical knowledge gap for environmental health risk assessment. To address this gap, we developed a mouse model subjected to coexposure to heat stress (36 °C, 4 h/day) and well-characterized polystyrene nanoplastics (PS-NPs, 60 nm, 10 mg/kg/day) for 30 consecutive days. Multidisciplinary approaches, including behavioral testing, histopathological analysis and molecular profiling, were employed to assess cognitive dysfunction and its underlying mechanisms. Compared with the single-exposure groups, coexposure induced pronounced cognitive deficits in mice, which were concomitant with hippocampal neurodegeneration, bloodbrain barrier (BBB) compromise, and exacerbated hippocampal oxidative stress. Transcriptomic profiling and subsequent validation revealed a novel role for oxidative stress-induced NLR family pyrin domain containing 6 (NLRP6) inflammasome activation in driving microglial pyroptosis, which exacerbates neuroinflammation through a feedforward loop. The administration of the antioxidant N-acetylcysteine (NAC) attenuated these pathological alterations by suppressing oxidative damage, thereby rescuing cognitive performance. This study elucidates a novel mechanism whereby heat stress and PS-NP coexposure synergistically disrupt neurological homeostasis via redox-sensitive inflammatory pathways, offering critical insights for the development of preventive strategies against combined environmental neurotoxicity.
More Papers Like This
Co-exposure to ozone and polystyrene nanoplastic exacerbates cognitive impairment and anxiety-like behavior by regulating neuronal pyroptosis in mice
AI summary Read the abstract
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 nanoplastics exposure induces cognitive impairment in mice via induction of oxidative stress and ERK/MAPK-mediated neuronal cuproptosis
AI summary Read the abstract
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.
Polystyrene nanoplastics induce hippocampal damage and cognitive deficits through oxidative stress-triggered microglial extracellular traps and neuronal ferroptosis
AI summary Read the abstract
Researchers showed that polystyrene nanoplastics impair spatial memory in mice by triggering a cascade in which hippocampal oxidative stress activates microglia to release extracellular traps, sustaining neuroinflammation that drives neuronal ferroptosis — a form of iron-dependent cell death — and that the antioxidant N-acetylcysteine blocks this entire pathway and preserves cognitive function.
Co-exposure to polystyrene nanoplastics and glyphosate exacerbates NETs-mediated pyroptosis by activating the NLRP3 inflammasome in mouse liver
AI summary Read the abstract
Researchers found that co-exposing mice to polystyrene nanoplastics and the herbicide glyphosate caused significantly worse liver damage than either pollutant alone. The combined exposure triggered a chain of inflammatory events including immune cell infiltration, formation of neutrophil traps, and cell death in liver tissue, all driven by activation of a key inflammatory pathway called NLRP3. The study suggests that nanoplastics may amplify the harmful effects of common agricultural chemicals when they enter the body together.
Short-term PS-NP exposure in early adulthood induces neuronal damage in middle-aged mice via microglia-mediated neuroinflammation
AI summary Read the abstract
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.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.