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Microglial clearance of Alzheimer's amyloid-beta obstructed by nanoplastics
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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.
Understanding the neurological impact of nanoplastic exposure has become an area of intensive research recently. This study examined the molecular and cellular mechanisms of how nanoplastics affect amyloid-beta (Aβ) clearance by microglia in the context of Alzheimer's disease (AD). Transmission electron microscopy and molecular dynamics simulations showed that polystyrene nanoplastics accelerated Aβ aggregation by forming a protein corona, promoting peptide fibrillization through hydrogen bonding and π-π interactions. Flow cytometry and endocytosis inhibition assays revealed that polystyrene nanoplastics impaired microglial uptake of Aβ while increasing their own cellular internalization, leading to microglial energy depletion and allowing Aβ aggregates to evade immune clearance. Additionally, proteomic analysis indicated that polystyrene nanoplastics disrupted microglial homeostasis, exacerbated neuroinflammation and metabolic dysregulation, and impaired the signalling pathway of ABC transporters critical for Aβ clearance in the AD brain. These findings suggest that nanoplastics contribute to AD pathology by impeding Aβ clearance and corrupting neuroimmune defense.
More Papers Like This
Impact of nanoplastics on Alzheimer ’s disease: Enhanced amyloid-β peptide aggregation and augmented neurotoxicity
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Researchers found that even very low concentrations of polystyrene nanoplastics can speed up the clumping of amyloid-beta protein, a hallmark of Alzheimer's disease, and increase its toxicity to brain cells. The hydrophobic (water-repelling) surface of the nanoplastics helps the proteins stick together faster, suggesting a potential link between environmental nanoplastic exposure and increased risk 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.
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.
Cerebral to Systemic Representations of Alzheimer’s Pathogenesis Stimulated by Polystyrene Nanoplastics
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Researchers found that environmentally realistic levels of polystyrene nanoplastics worsened Alzheimer's disease symptoms in mice, triggering brain inflammation, neuron death, and cognitive decline. The nanoplastics also disrupted metabolism and caused organ damage beyond the brain, including liver and kidney effects. This study provides some of the first evidence that nanoplastic exposure could accelerate brain diseases like Alzheimer's, especially as nanoplastics have been found in human brain tissue.
Nanoplastics trigger glial–neuronal collagen signaling miscommunication to exacerbate cognitive impairment in Alzheimer's disease
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Researchers found that polystyrene nanoplastics worsen cognitive impairment in Alzheimer's disease mouse models by disrupting communication between glial cells and neurons through the collagen-integrin signaling pathway. The study showed that nanoplastics triggered astrocytes and microglia to produce excess collagen, driving neurotoxicity. A drug blocking collagen signaling rescued cognitive function in nanoplastic-exposed Alzheimer's mice, and the same collagen pathway was found to be upregulated in human Alzheimer's brains.
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