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Effects of Microplastic Accumulation on Neuronal Death After Global Cerebral Ischemia
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Researchers found that microplastics worsened brain damage after a stroke-like event in mice, increasing inflammation, damaging the protective coating around nerve fibers, and causing more brain cell death. The microplastics also triggered the release of abnormal tau proteins, similar to what happens in Alzheimer's disease, suggesting that microplastic exposure could make the brain more vulnerable to injury and neurodegenerative conditions.
Brain ischemia, a condition in which the brain is deprived of blood flow, can lead to a stroke due to blocked or unstable blood vessels. Global cerebral ischemia (GCI), characterized by an interruption in blood flow, deprives the brain of oxygen and nutrients, producing reactive oxygen species (ROS) that trigger cell death, which kills nerve cells. Microplastics (MPs), tiny environmental pollutants, can enter the human body through contaminated food, water, disposable items, cosmetics, and more. Once in the brain, MPs can increase neuroinflammation by overstimulating inflammatory factors such as microglia. MPs can also damage neurons by scratching myelin and microtubules, slowing signal transduction, causing cognitive impairment, and leading to neuronal death. Furthermore, microtubule damage may result in the release of phosphorylated tau proteins, potentially linked to Alzheimer's disease. We hypothesized that MPs could exacerbate neuroinflammation and microtubule destruction after GCI, leading to increased neuronal death. To test this hypothesis, we administered MPs (0.5 µm) orally at a dose of 50 mg/kg before and after inducing GCI. Staining techniques such as Fluoro-Jade B (FJB), ionized calcium-binding adaptor molecule 1 (Iba-1), cluster of differentiation 68 (CD68), myelin basic protein (MBP), and microtubule-associated protein 2 (MAP2) were used, along with Western blot analysis for interleukin-6 (IL-6), TNF-α, tau-5, and phospho-tau (S396) to evaluate the effects of MPs on neuronal cell death, neuroinflammation, and microtubule destruction. The results showed that MP accumulation significantly increased neuroinflammation, microtubule disruption, and neuronal cell death in the GCI-MP group compared to the GCI-vehicle group. Therefore, this study suggests that MP accumulation in daily life may contribute to the exacerbation of the disease, potentially leading to severe neuronal cell death after GCI.
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Exposure to Polystyrene Microplastics Promotes the Progression of Cognitive Impairment in Alzheimer’s Disease: Association with Induction of Microglial Pyroptosis
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In a mouse study, polystyrene microplastics worsened cognitive decline in an Alzheimer's disease model by triggering a type of inflammatory cell death called pyroptosis in brain immune cells. The microplastics caused brain inflammation that accelerated memory loss and cognitive impairment beyond what Alzheimer's alone caused. This is one of the first studies suggesting that microplastic exposure could make neurodegenerative diseases like Alzheimer's progress faster.
Short-Term Exposure to Polystyrene Microplastics Alters Cognition, Immune, and Metabolic Markers in an APOE Genotype and Sex-Dependent Manner
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Researchers exposed Alzheimer's disease mouse models to polystyrene microplastics for a short term and observed worsened cognitive performance, altered immune markers, and disrupted metabolic pathways, suggesting that MP exposure may accelerate neurological decline in individuals already vulnerable to dementia.
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.
The Effect of Microplastics Exposure on Alzheimer’s Disease Pathology Characterized using APP/PSEN1 Mice
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Researchers chronically exposed APP/PSEN1 Alzheimer's disease model mice to polystyrene nano- and microplastics and found preliminary evidence that exposure worsens cognitive impairment and increases amyloid-beta plaque accumulation, building on prior work showing NMP effects in APOE4 mice and suggesting plastic particles may accelerate neurodegenerative disease progression.
Nanoplastics exposure exacerbates Aβ plaque deposition in Alzheimer’s disease mice by inducing microglia pyroptosis
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In Alzheimer's disease model mice, exposure to environmentally relevant doses of nanoplastics worsened cognitive problems and increased the brain plaques associated with the disease. The nanoplastics damaged a waste-clearing system in brain immune cells called microglia, reducing their ability to remove harmful amyloid plaques, though the study also found that melatonin treatment helped restore brain cell function and reduce plaque buildup.
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