Anionic nanoplastic contaminants promote Parkinson’s disease–associated α-synuclein aggregation

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Nanoplastics in brain linked to Parkinson’s disease, dementia proteins

Scientists find that the presence of extremely small plastic particles, called nanoplastics, in mouse brains appears to be linked to formation of proteins associated with development of Parkinson’s disease and related dementias. Mice, humans, and other animals collect plastic particles in their bodies when they eat, drink, and breathe. Some plastic particles may even be absorbed by the skin.

Abstract: Recent studies have identified increasing levels of nanoplastic pollution in the environment. Here, we find that anionic nanoplastic contaminants potently precipitate the formation and propagation of α-synuclein protein fibrils through a high-affinity interaction with the amphipathic and non-amyloid component (NAC) domains in α-synuclein. Nanoplastics can internalize in neurons through clathrin-dependent endocytosis, causing a mild lysosomal impairment that slows the degradation of aggregated α-synuclein. In mice, nanoplastics combine with α-synuclein fibrils to exacerbate the spread of α-synuclein pathology across interconnected vulnerable brain regions, including the strong induction of α-synuclein inclusions in dopaminergic neurons in the substantia nigra. These results highlight a potential link for further exploration between nanoplastic pollution and α-synuclein aggregation associated with Parkinson’s disease and related dementias.

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