Targeting prion-like protein spreading in neurodegenerative diseases

Zhaohui Zhang, Shuke Nie, Liam Chen

Research output: Contribution to journalReview articlepeer-review

16 Scopus citations


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 cellto-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.

Original languageEnglish (US)
Pages (from-to)1875-1878
Number of pages4
JournalNeural Regeneration Research
Issue number11
StatePublished - 2018
Externally publishedYes

Bibliographical note

Funding Information:
We thank Dr. Xiaobo Mao (Johns Hopkins University School of Medicine) for constructive comments.

Publisher Copyright:
© 2018 Medknow. All rights reserved.


  • Alzheimer's disease
  • Parkinson's disease
  • TAR DNA-binding protein 43
  • amyotrophic lateral sclerosis
  • beta-amyloid
  • frontotemporal dementia
  • neurodegeneration
  • prion-like
  • synuclein
  • tau


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