中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (11): 1875-1878.doi: 10.4103/1673-5374.239433

• 综述:退行性病与再生 • 上一篇    下一篇

靶向朊病毒蛋白在神经退行性疾病中的传播

  

  • 收稿日期:2018-07-23 出版日期:2018-11-15 发布日期:2018-11-15

Targeting prion-like protein spreading in neurodegenerative diseases

Zhaohui Zhang1, Shuke Nie1, 2, Liam Chen2   

  1. 1 Department of Neurology, Renmin Hospital, Wuhan University, Wuhan, Hubei Province, China
    2 Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • Received:2018-07-23 Online:2018-11-15 Published:2018-11-15
  • Contact: Liam Chen, MD, PhD,lchen99@jhmi.edu.

摘要:

orcid:0000-0001-5553-5473(Liam Chen)

Abstract:

The infectious template-mediated protein conversion is a unique mechanism for the onset of rare and fatal neurodegenerative disorders known as transmissible spongiform encephalopathies, or prion diseases, which affect humans and other animal species. However, emerging studies are now demonstrating prion-like mechanisms of self-propagation of protein misfolding in a number of common, non-infectious neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. It has been proposed that distinct and unrelated proteins (beta-amyloid, tau, α-synuclein, TAR DNA-binding protein 43 and huntingtin, etc.) associated with common neurodegenerative disorders can seed conversion and spread via cell-to-cell transfer, sustaining the transmission of neurotoxic agents along a stereotypic route, sharing features at the heart of the intrinsic nature of prions. Here we review the most recent development on both the molecular mechanisms underlying the pathogenesis of prion-like neurodegenerative diseases as well as innovative methods and strategies for potential therapeutic applications.

Key words: prion-like, synuclein, tau, TAR DNA-binding protein 43, beta-amyloid, Parkinson’s disease, frontotemporal dementia, amyotrophic lateral sclerosis, Alzheimer’s disease, neurodegeneration