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at 24 h) with assessments of DNA damage and inflammatory responses. Functionally, GQDs destabilized preformed ASN fibrils in a cell-free assay, as evidenced by reduced Thioflavin-T fluorescence. In primary murine dopaminergic neurons, GQDs decrease pS129-ASN inclusion formation without compromising neuronal viability. Most importantly, intranasal administration of GQDs in an MSA mouse model reduced ASN immunoreactivity in the brain. Collectively, our data indicate that the synthetized GQDs are bioactive and can modulate ASN aggregation across cell-free, neuronal, and in vivo models. Importantly, physicochemical properties govern nano - bio interactions, providing a rationale for further refinement of GQDs as a biomaterial platform for synucleinopathy-related applications.
Öz et al. (Thu,) studied this question.