We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Identification of ceRNA network to explain the mechanism of cognitive dysfunctions induced by PS NPs in mice
AI summary Read the abstract
Researchers exposed mice to polystyrene nanoplastics for six months and found dose-dependent cognitive decline along with increased oxidative stress and DNA damage in the prefrontal cortex. The study identified a competing endogenous RNA network involving circRNAs, miRNAs, and mRNAs that may explain the molecular mechanism behind nanoplastic-induced neurotoxicity.
Plastics breaking down of larger plastics into smaller ones (microplastics and nanoplastic) as potential threats to the ecosystem. Previous studies demonstrate that the central nervous system (CNS) is a vulnerable target of nanoplastics. However, the potentially epigenetic biomarkers of nanoplastic neurotoxicity in rodent models are still unknown. The present research aimed to determine the role of competing endogenous RNA (ceRNA) in the process of polystyrene nanoplastics (PS NPs) exposure-induced nerve injury. The study was designed to investigate whether 25 nm PS NPs could cause learning dysfunction and to elucidate the underlying mechanisms in mice. A total of 40 mice were divided into 4 groups and were exposed to PS NPs (0, 10, 25, 50 mg/kg). Chronic toxicity was introduced in mice by administration of oral gavage for 6 months. The evaluation included assessment of their behavior, pathological investigation and determination of the levels of reactive oxygen species (ROS) and DNA damage. RNA-Seq was performed to detect the expression levels of circRNAs, miRNAs and mRNAs in PFC samples of mice treated with 0 and 50 mg/kg PS NPs. The results indicated that exposure of mice to PS NPs caused a dose-dependent cognitive decline. ROS levels and DNA damage were increased in the PFC following exposure of the mice to PS NPs. A total of 987 mRNAs, 29 miRNAs and 67 circRNAs demonstrated significant differences between the 0 and 50 mg/kg PS NPs groups. Functional enrichment analyses indicated that PS NPs may induce major injury in the synaptic function. A total of 96 mRNAs, which were associated with synaptic dysfunction were identified. A competing endogenous RNA (ceRNA) network containing 27 circRNAs, 19 miRNAs and 35 synaptic dysfunction-related mRNAs was constructed. The present study provided insight into the molecular events associated with nanoplastic toxicity and induction of cognitive dysfunction.
More Papers Like This
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.
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.
Comprehensive Analysis of lncRNA–mRNA Expression Profiles in Depression-like Responses of Mice Related to Polystyrene Nanoparticle Exposure
AI summary Read the abstract
Researchers found that polystyrene nanoparticle exposure induced depression-like behaviors in mice and identified altered long non-coding RNA and mRNA expression profiles in brain tissue, revealing molecular pathways through which nanoplastics may affect neurological function.
Polystyrene nanoplastics induce cognitive dysfunction and dendritic spine deterioration via excessive mitochondrial fission
AI summary Read the abstract
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 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.
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.