Targeting prion-like protein spreading in neurodegenerative diseases

Zhaohui Zhang, Shuke Nie, Liam Lucian Chen

Research output: Contribution to journalReview article

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 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
Volume13
Issue number11
DOIs
Publication statusPublished - Jan 1 2018

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Keywords

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

ASJC Scopus subject areas

  • Developmental Neuroscience

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