Of the fastest growing neurological disorders in the world, Parkinson’s disease is pathologically defined by the accumulation of the protein α-synuclein in vulnerable neurons in the brain. Prolonged exposure to environmental challenges of largely unknown origins are suspected as principal driving factors for disease risk and progression. The increase in polystyrene nanoplastics in the environment from single-use plastics, recent detection of polystyrene contaminants in blood, and reports of anionic polystyrene plastics disrupting and crossing the blood-brain barrier indicated nanoplastics as a relevant class of pollutant to explore for interaction with α-synuclein. The research team, including Addison Duda (Franz Lab) and Dr. Ben Bobay (NMR Facility), highlights the emergent potential toxin of anionic nanoplastics as having a possible role in Parkinson’s disease risk and progression. They found that anionic nanoplastic contaminants potently precipitate the formation and propagation of pathological α-synuclein protein fibrils through a high-affinity interaction with the amphipathic and non-amyloid component (NAC) domains in α-synuclein. They revealed and quantified stabilization of anionic polystyrene complex through strong electrostatic attraction between protein lysines and nanoplastic carboxylates. In mice, the anionic nanoplastics combine with α-synuclein fibrils to exacerbate the spread of α-synuclein pathology across interconnected vulnerable brain regions. The results highlight a potential link for further exploration between nanoplastic pollution and α-synuclein aggregation associated with Parkinson’s disease and related dementias. Read more about this exciting collaboration with the West Lab in Pharmacology and Cancer Biology in a recent Science Advances article, available here.
Chemistry
