Nanozyme scavenging ROS for prevention of pathologic α-synuclein transmission in Parkinson's disease

Yu Qing Liu, Yuanyang Mao, Enquan Xu, Huimin Jia, Shu Zhang, Valina L. Dawson, Ted M. Dawson, Yan Mei Li, Zhi Zheng, Weiwei He, Xiaobo Mao

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


Braak's prion-like theory fundamentally subverts the understanding of Parkinson's disease (PD). Emerging evidence shows that pathologic α-synuclein (α-syn) is a prion-like protein that spreads from one region to another in PD brain, which is an essential driver to the pathogenesis of PD. Thus far, there is a big knowledge gap that limited nanomaterial that can block prion-like spreading. Here, α-syn preformed fibrils (PFF) are used to model prion-like spreading and biocompatible antioxidant nanozyme, PtCu nanoalloys (NAs), is applied to fight against α-syn spreading. The results show that PtCu NAs significantly inhibit α-syn pathology, cell death, and neuron-to-neuron transmission by scavenging reactive oxygen species (ROS) in primary neuron cultures. Moreover, the PtCu NAs significantly inhibit α-syn spreading induced by intrastriatal injection of PFF. It is the first time to observe nanozyme can block prion-like spreading, which provides a proof of concept for nanozyme therapy. It is also anticipated that the biomedical application of nanozyme against prion-like spreading could be optimized and considered to be developed as a therapeutic strategy against Parkinson's disease, Alzheimer's disease, and other prion-like proteinopathies.

Original languageEnglish (US)
Article number101027
JournalNano Today
StatePublished - Feb 2021


  • Cell-to-cell transmission
  • Nanozyme
  • Parkinson's disease
  • Prion-like
  • α-Synuclein

ASJC Scopus subject areas

  • Biotechnology
  • Bioengineering
  • Biomedical Engineering
  • Materials Science(all)
  • Pharmaceutical Science


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