Cited by 185Alzheimer's disease research and treatmentsPrion Diseases and Protein MisfoldingParkinson's Disease Mechanisms and Treatments

Prion-like spread of protein aggregates in neurodegeneration

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Polymenidou, Magdalini, Cleveland, Don W.·2012·Journal of Experimental Medicine

Abstract

Protein misfolding is common to most neurodegenerative diseases, including Alzheimer’s and Parkinson’s diseases. Recent work using animal models with intracellular α-synuclein and tau inclusions adds decisively to a growing body of evidence that misfolded protein aggregates can induce a self-perpetuating process that leads to amplification and spreading of pathological protein assemblies. When coupled with the progressive nature of neurodegeneration, recognition of such cell-to-cell aggregate spread suggests a unifying mechanism underlying the pathogenesis of these disorders.

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  • There is substantial evidence that propagation of pathological tau species occurs between cells.

    “While still a contentious topic [46], there is now substantial evidence that also supports the idea that propagation of pathological tau species occurs between cells [47–50].”

    From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [49]

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  1. Kato M. Han T. Xie S. Shi K. Du X. Wu L. Mirzaei H. Goldsmith E. Longgood J. Pei J. 2012 Cell-free formation of RNA granules: LCS domains of protein components polymerize forming hydrogels. Cell. In press

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Authors
Polymenidou, M., & Cleveland, D. W.
Affiliations
Ludwig Cancer Research (BE)
Corresponding author
Cleveland, Don W.
Venue
Journal of Experimental Medicine
Published
2012-05-07
Volume
209
Issue
5
Pages
889-893
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2113281193
Cited by
184
References
40
Citations by year
2026: 5 · 2025: 8 · 2024: 4 · 2023: 7 · 2022: 4 · 2021: 5 · 2020: 7 · 2019: 11 · 2018: 13 · 2017: 14 · 2016: 24 · 2015: 22 · 2014: 23 · 2013: 29 · 2012: 7
FWCI
2.82
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Funders
  • Wellcome Trust (089701)
  • National Institute of Neurological Disorders and Stroke (R37 NS 27036, K99NS075216, R37NS027036)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords
prion-like spread, protein aggregates, protein misfolding, neurodegeneration, Alzheimer's disease, Parkinson's disease, alpha-synuclein, tau protein, cell-to-cell transmission, animal models
MeSH terms
Animals, Humans, Prions, Neurofibrillary Tangles, tau Proteins, Neurodegenerative Diseases, Mice, alpha-Synuclein, Proteostasis Deficiencies

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