黑质
帕金森病
α-突触核蛋白
纤维
内吞作用
多巴胺能
淀粉样纤维
淀粉样蛋白(真菌学)
生物物理学
化学
蛋白质聚集
细胞生物学
疾病
神经科学
多巴胺
淀粉样β
生物
生物化学
医学
内科学
细胞
无机化学
作者
Zhiyong Liu,Arpine Sokratian,Addison M. Duda,Enquan Xu,Christina M Stanhope,A Fu,Samuel Strader,H. Li,Yuan Yuan,Benjamin G. Bobay,Joana Marie Sipe,Keliya Bai,Iben Lundgaard,Na Liu,Belén Hernández,Catherine Bowes Rickman,Sara Miller,Andrew B. West
出处
期刊:Science Advances
[American Association for the Advancement of Science (AAAS)]
日期:2023-11-15
卷期号:9 (46)
被引量:6
标识
DOI:10.1126/sciadv.adi8716
摘要
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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