We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Short-term PS-NP exposure in early adulthood induces neuronal damage in middle-aged mice via microglia-mediated neuroinflammation
Summary
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.
Nanoplastics (NPs) are ubiquitous environmental pollutants that have garnered considerable attention for their potential adverse health effects. In this study, male C57BL/6 J mice were orally treated with a mixture of 50-nm and 200-nm polystyrene (PS)-NPs for one week followed by measurements of their neurobehavioral performance and neuronal damage 10 months later. Notably, PS-NPs were detected in the brains of the mice by transmission electron microscopy (TEM) and a nanoscale hyperspectral microscope imaging system 10 months after the PS-NP exposure. The mice exposed to short-term PS-NPs exhibited cognitive dysfunction and anxiety-like symptoms, neuronal damage and synapse loss, and an increase in the number of M1-polarized microglia and A1-reactive astrocytes. Interestingly, the inhibition of microglial activation by minocycline significantly mitigated the PS-NP-induced synapse loss and neuron damage. In vitro studies showed that PS-NPs could be readily internalized by three types of neurovascular unit (NVU) cells, including microglia, astrocytes, and brain microvascular endothelial cells, via multiple pathways. RNA-seq analysis confirmed that microglia-mediated neuronal injury was associated with disturbances in synapse and cell death signaling pathways. Collectively, these findings suggest that short-term PS-NP exposure-induced neuroinflammation in early adulthood may not be resolved naturally but may deteriorate under the interaction of microglia and astrocytes, leading to synapse loss, neuron degeneration, and cognitive dysfunction in middle age. The results of the present study provide important insights into the potential neurological impacts of NPs and suggest that targeting microglia to suppress inflammation might be a potential intervention strategy for neurodegeneration induced by NPs.
Sign in to start a discussion.
More Papers Like This
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.
Lifelong exposure to polystyrene-nanoplastics induces an attention-deficit hyperactivity disorder-like phenotype and impairs brain aging in mice
Mice exposed to nanoplastics throughout their entire lives -- from the womb through old age -- developed ADHD-like symptoms as adults, including hyperactivity, risk-taking behavior, and impaired learning, and showed a lower seizure threshold in old age. These behavioral changes were accompanied by altered brain proteins and accelerated brain aging at the cellular level, suggesting lifelong nanoplastic exposure may contribute to neurodevelopmental and neurodegenerative disorders.
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.
Cerebral to SystemicRepresentations of Alzheimer’sPathogenesis Stimulated by Polystyrene Nanoplastics
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.
Polystyrene nanoplastics penetrate across the blood-brain barrier and induce activation of microglia in the brain of mice
Researchers demonstrated that 50-nanometer polystyrene nanoplastics can cross the blood-brain barrier in mice, accumulate in brain tissue, and activate immune cells called microglia that then damage neurons. The nanoplastics disrupted the tight junctions that normally protect the brain, creating openings for the particles to pass through. This study provides direct evidence that nanoplastics can reach the brain and trigger inflammation, raising concerns about potential neurological effects of long-term nanoplastic exposure in humans.