黑质
帕金森病
纤维
α-突触核蛋白
多巴胺能
内吞作用
淀粉样纤维
淀粉样蛋白(真菌学)
化学
疾病
细胞生物学
生物物理学
神经科学
多巴胺
淀粉样β
生物
生物化学
内科学
医学
细胞
无机化学
作者
Yong Li,Arpine Sokratian,Addison M. Duda,Enquan Xu,Christina M Stanhope,Amy Kit Yu Fu,Samuel Strader,Huizhong Li,Yuan Yuan,Benjamin G. Bobay,Jean D. Sipe,Keliya Bai,Iben Lundgaard,Na Liu,Belinda Hernández,Catherine Bowes Rickman,Sara Miller,Andrew B. West
出处
期刊:Research Square - Research Square
日期:2023-10-13
标识
DOI:10.21203/rs.3.rs-3439102/v1
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI