We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Murine hippocampal CA3 vulnerability to intravenously administered polystyrene nanoplastics: preferential accumulation and ROS-related neuronal cell death
AI summary Read the abstract
In mice injected with tiny polystyrene plastic particles, the particles built up mainly in a specific brain region (hippocampal CA3), where nerve cells died off and showed signs of oxidative stress. These mice also performed worse on memory and learning tests compared to untreated mice.
Polystyrene nanoplastics (PS-NPs) are emerging neurotoxicants with the potential to access the brain following systemic exposure; however, their region-specific effects and underlying mechanisms remain incompletely understood. In this study, adult male mice (C57BL/6J) were intravenously injected with unlabeled or fluorescently labeled PS-NPs (50-60 nm) at a dose of 400 mg/kg, and brain tissues were collected and analyzed 3 days post-injection to evaluate PS-NPs distribution, oxidative stress, and regulated cell death pathways. Confocal imaging revealed preferential accumulation of fluorescent PS-NPs in the hippocampal CA3 region, where neuronal localization was most prominent among the regions examined. This accumulation was associated with a significant reduction in NeuN-positive neurons in CA3 (p < 0.01), accompanied by elevated mitochondrial ROS levels as detected by MitoSOX staining (p < 0.001). Immunofluorescence analyses demonstrated increased expression of cleaved caspase-3 and p-MLKL, indicating activation of apoptosis and necroptosis, whereas NLRP3 expression remained unchanged. Behavioral assessments using the Y-maze and passive avoidance tests revealed impairments in hippocampus-dependent cognitive performance in PS-NP-treated mice. Collectively, these findings suggest that acute intravenous exposure to PS-NPs induces early, region-selective neuronal vulnerability in the hippocampal CA3 area, which is associated with oxidative stress-mediated neuronal cell death and cognitive dysfunction under the present experimental conditions.
More Papers Like This
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.
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.
Cerebral to SystemicRepresentations of Alzheimer’sPathogenesis Stimulated by Polystyrene Nanoplastics
AI summary Read the abstract
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.
Neurotoxic potential of polystyrene nanoplastics in primary cells originating from mouse brain
AI summary Read the abstract
Researchers exposed three types of primary mouse brain cells to 100 nm polystyrene nanoplastics and found that neurons underwent apoptosis while astrocytes survived but developed reactive astrocytosis with elevated inflammatory markers, suggesting that neuronal vulnerability to nanoplastic accumulation may be amplified by astrocyte-driven neuroinflammation.
Manifestation of polystyrene microplastic accumulation in brain with emphasis on morphometric and histopathological changes in limbic areas of Swiss albino mice
AI summary Read the abstract
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.
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.