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Cerebral neurotoxicity of amino-modified polystyrene nanoplastics in mice and the protective effects of functional food Camellia pollen
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Mice exposed long term to amino-modified polystyrene nanoplastics had the particles in brain tissue, along with higher activity of two genes associated with Alzheimer's disease. In cell experiments, the particles disrupted proteins that seal the blood-brain barrier and promoted a modified form of tau. Camellia pollen reduced these effects in the cell models.
Accumulating evidence suggests that nanoplastics contribute to an increased risk of brain damage, however, the precise underlying mechanisms remain unclear. Here, we subjected mice to long-term exposure to amino-modified polystyrene nanoplastics (APS-NPs). These nanoplastics were detected in the mouse brain; coupled with the observed upregulation of Alzheimer's disease-associated genes (APP and MAPT). To further explore nanoplastic damage mechanisms and the corresponding protective strategies against these mechanisms in vitro, we used hCMEC/D3 and HT22 cells. Results showed that APS-NPs disrupted tight junction proteins (Occludin and ZO-1) via TLR2/MMP9 axis, resulting in blood-brain barrier permeation; this was significantly mitigated by functional food Camellia pollen treatment. APS-NPs initiated iNOS and nNOS upregulation within neurons resulting in Sirtuin 1 deacetylase inactivation and CBP acetyltransferase stimulation, ultimately leading to Ac-Tau formation. This process was attenuated by Camellia pollen, which also ameliorated the APS-NPs-induced neuronal apoptosis mediated by the p53/Bax/Bcl-2 axis. Network pharmacology analysis of Camellia pollen offered a further theoretical understanding of its potential applications in preventing and treating nervous system disorders, such as Alzheimer's disease. This study established that Camellia pollen protects the brain against APS-NPs-mediated blood-brain barrier damage and alleviates neuronal apoptosis and Alzheimer's disease-like neurotoxicity. This study elucidates the mechanisms underlying polystyrene-induced brain damage and can be used to inform future prevention and treatment strategies.
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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.
Cerebral to SystemicRepresentations of Alzheimer’sPathogenesis Stimulated by Polystyrene Nanoplastics
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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.
Micro- and Nanoplastics and Functional Nutrients in Human Health: Epigenetic Mechanisms and Cellular Resilience Signaling in Brain Insulin Resistance and the Risk of Alzheimer’s Disease
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This review explores how functional nutrients like polyphenols and flavonoids may help counteract damage caused by micro- and nanoplastic exposure, particularly regarding brain health. The study suggests these nutrients can activate protective cellular pathways at low doses to help maintain blood-brain barrier integrity, though chronic pollutant exposure may disrupt antioxidant signaling and contribute to brain insulin resistance.
Research progress in mechanisms of neurotoxicity induced by micro(nano)plastic exposure
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This review examines how micro- and nanoplastics may harm the nervous system, through oxidative stress, mitochondrial damage, a disrupted blood-brain barrier and the gut-brain axis. It also notes early studies of substances tested against these effects, including curcumin, probiotics and Camellia pollen. Chronic low-dose exposure remains a research gap.
Polystyrene nanoplastics induce hippocampal damage and cognitive deficits through oxidative stress-triggered microglial extracellular traps and neuronal ferroptosis
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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.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.