The Effect of Polyethylene Terephthalate Nanoplastics on Amyloid-β Peptide Fibrillation

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 (PET50nm and PET140nm) and concentrations (0, 10, 50, and 100 ppm) on the fibrillation of Aβ1-40. Our results showed that the presence of PET50nm as well as PET140nm 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 PET50nm and 3.8 ± 0.06 h for PET140nm. 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 the presence of 100 ppm PET50nm. These changes indicate that higher concentrations (100 ppm) of PET50nm promote more rigid and uniform peptide aggregates. Although PET50nm NPs influence the kinetics of aggregation and secondary structure, the overall morphology of the resulting fibrils remains largely unaltered, as seen using transmission electron microscopy. Also, the local cross-β structure of the fibrils was not affected by the presence of PET50nm NPs during fibrillation, as confirmed using 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.