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 (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.