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
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,Huizhong Li,Yuan Yuan,Benjamin G. Bobay,Joana Marie Sipe,Ketty Bai,Iben Lundgaard,Na Liu,B. 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:2023-11-17
卷期号:9 (46)
被引量:41
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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