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
StatePublished - Jan 1 2018

Fingerprint

Neurodegenerative Diseases
Prions
Prion Diseases
Synucleins
Amyloid beta-Peptides
DNA-Binding Proteins
Parkinson Disease
Seeds
Alzheimer Disease
Proteins
Prion Proteins
Therapeutics

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

Cite this

Targeting prion-like protein spreading in neurodegenerative diseases. / Zhang, Zhaohui; Nie, Shuke; Chen, Liam Lucian.

In: Neural Regeneration Research, Vol. 13, No. 11, 01.01.2018, p. 1875-1878.

Research output: Contribution to journalReview article

@article{1c88798cde1e4fe68d406b7270f1eaad,
title = "Targeting prion-like protein spreading in neurodegenerative diseases",
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.",
keywords = "Alzheimer's disease, amyotrophic lateral sclerosis, beta-amyloid, frontotemporal dementia, neurodegeneration, Parkinson's disease, prion-like, synuclein, TAR DNA-binding protein 43, tau",
author = "Zhaohui Zhang and Shuke Nie and Chen, {Liam Lucian}",
year = "2018",
month = "1",
day = "1",
doi = "10.4103/1673-5374.239433",
language = "English (US)",
volume = "13",
pages = "1875--1878",
journal = "Neural Regeneration Research",
issn = "1673-5374",
publisher = "Editorial Board of Neural Regeneration Research",
number = "11",

}

TY - JOUR

T1 - Targeting prion-like protein spreading in neurodegenerative diseases

AU - Zhang, Zhaohui

AU - Nie, Shuke

AU - Chen, Liam Lucian

PY - 2018/1/1

Y1 - 2018/1/1

N2 - 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.

AB - 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.

KW - Alzheimer's disease

KW - amyotrophic lateral sclerosis

KW - beta-amyloid

KW - frontotemporal dementia

KW - neurodegeneration

KW - Parkinson's disease

KW - prion-like

KW - synuclein

KW - TAR DNA-binding protein 43

KW - tau

UR - http://www.scopus.com/inward/record.url?scp=85060661486&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85060661486&partnerID=8YFLogxK

U2 - 10.4103/1673-5374.239433

DO - 10.4103/1673-5374.239433

M3 - Review article

C2 - 30233055

AN - SCOPUS:85060661486

VL - 13

SP - 1875

EP - 1878

JO - Neural Regeneration Research

JF - Neural Regeneration Research

SN - 1673-5374

IS - 11

ER -