Prion-like spread of protein aggregates in neurodegeneration
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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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- Authors
- Polymenidou, M., & Cleveland, D. W.
- Affiliations
- Ludwig Cancer Research (BE)
- Corresponding author
- Cleveland, Don W.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2012-05-07
- Volume
- 209
- Issue
- 5
- Pages
- 889-893
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC3348110
- 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
- green
- www.ncbi.nlm.nih.gov
- 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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