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The Effect of Polyethylene Terephthalate Nanoplastics on Amyloid-β Peptide Fibrillation
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Researchers investigated whether PET nanoplastics (50 nm and 140 nm) affect the fibrillation of amyloid-beta peptides associated with Alzheimer's disease pathology. PET nanoplastics at concentrations of 10–100 ppm influenced Aβ aggregation kinetics in a size- and concentration-dependent manner, adding to evidence that nanoplastics reaching the brain may modulate neurodegenerative protein aggregation.
Exposure of organisms to nanoplastics (NPs) is inevitable given their global abundance and environmental persistence. Polyethylene terephthalate (PET) is a common plastic used in a wide range of products, including clothing and food and beverage packaging. Recent studies suggest that NPs can cross the blood-brain barrier and cause potential neurotoxicity. It is widely known that aggregation of amyloid beta (Aβ) peptides in the brain is a pathological hallmark of Alzheimer's disease (AD). While the impact of nanoplastics such as polystyrene (PS) on amyloid aggregation has been studied, the effects of PET NPs remain unexplored. In this study, we examined the effect of PET NPs of different sizes (PET50 nm and PET140 nm) and concentrations (0, 10, 50 and 100 ppm) on the fibrillation of Aβ1-40. Our results showed that the presence of PET50 nm as well as PET140 nm decreased the lag phase of the fibrillation processes in a dose- and size-dependent manner from 6.7 ± 0.08 h for Aβ in the absence of PET (Aβcontrol) to 3.1 ± 0.03 h for PET50 nm and 3.8 ± 0.06 h for PET140 nm. CD spectroscopy showed that PET50nm significantly impacts the structural composition of Aβ aggregates. A significant rise in antiparallel β-sheet content and β-turn structure and a substantial reduction in other structures were observed in presence of 100 ppm PET50 nm. These changes indicate that higher concentrations (100 ppm) of PET50 nm promote more rigid and uniform peptide aggregats. Although PET50 nm NPs influence the kinetics of aggregation and secondary structure, the overall morphology of the resulting fibrils remains largely unaltered, as seen by transmission electron microscopy. Also the local cross-β structure of the fibrils was not affected by the presence of PET50 nm NPs during fibrillation, as confirmed by 13C solid-state NMR spectroscopy. Overall, these findings show that PET NPs accelerate amyloid fibril formation and alter the secondary structure of Aβ fibrils. These results also indicate that the accumulation of PET-NPs in the brain may facilitate the progression of various neurodegenerative diseases, including Alzheimer's disease.
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The Effect of Polyethylene Terephthalate Nanoplastics on Amyloid-β Peptide Fibrillation
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Lab experiments showed that PET nanoplastics, the type found in plastic bottles and clothing, accelerated the clumping of amyloid-beta proteins, which is a hallmark of Alzheimer's disease. Smaller nanoplastics (50 nm) had a stronger effect than larger ones, cutting the time for protein clumping nearly in half. While this is a test-tube study, it raises the question of whether nanoplastics that reach the brain could potentially speed up the development of Alzheimer's-related protein buildup.
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.
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Researchers used coarse-grained molecular dynamics simulations to study nanoplastic interactions with beta-amyloid fibrils, finding that nanoplastics can influence amyloid aggregation and potentially play a role in neurodegenerative disease pathways.
Protein aggregation, hydrophobicity and neurodegenerative disease
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This doctoral thesis on protein aggregation and neurodegenerative disease includes an important finding relevant to microplastics: nanoscale PET plastic particles were shown to accelerate the formation of amyloid fibrils from alpha-synuclein, a protein central to Parkinson's disease. This raises the concern that everyday nanoplastic exposure could contribute to the onset or progression of neurodegenerative conditions.
Micro/NanoplasticsDrive Amyloid-β Colloidaland Oxidative Reorganization: A Real-World Contaminant Stressor
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Scientists tested how tiny plastic particles from everyday plastic bottles (PET plastic) interact with amyloid-beta, a protein linked to Alzheimer's disease, in lab experiments. They found these microplastics did change the protein's shape and behavior over time and slightly increased oxidative stress (a type of cell damage), but the exact real-world implications aren't yet clear. This early-stage research suggests microplastics could potentially influence processes involved in Alzheimer's disease, but more studies are needed before we know what this means for actual human health risk.
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