Prion-like spreading of pathological α-synuclein in brain
Open accessAbstract
α-Synuclein is the major component of filamentous inclusions that constitute the defining characteristic of neurodegenerative α-synucleinopathies. However, the molecular mechanisms underlying α-synuclein accumulation and spread are unclear. Here we show that intracerebral injections of sarkosyl-insoluble α-synuclein from brains of patients with dementia with Lewy bodies induced hyperphosphorylated α-synuclein pathology in wild-type mice. Furthermore, injection of fibrils of recombinant human and mouse α-synuclein efficiently induced similar α-synuclein pathologies in wild-type mice. C57BL/6J mice injected with α-synuclein fibrils developed abundant Lewy body/Lewy neurite-like pathology, whereas mice injected with soluble α-synuclein did not. Immunoblot analysis demonstrated that endogenous mouse α-synuclein started to accumulate 3 months after inoculation, while injected human α-synuclein fibrils disappeared in about a week. These results indicate that α-synuclein fibrils have prion-like properties and inoculation into wild-type brain induces α-synuclein pathology in vivo. This is a new mouse model of sporadic α-synucleinopathy and should be useful for elucidating progression mechanisms and evaluating disease-modifying therapy.
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- Authors
- Masuda-Suzukake, M., Nonaka, T., Hosokawa, M., Oikawa, T., Arai, T., Akiyama, H., Mann, D. M. A., & Hasegawa, M.
- Affiliations
- Tokyo Metropolitan Institute of Medical Science (JP)
- University of Tsukuba (JP)
- University of Manchester (GB)
- Corresponding author
- Hasegawa, Masato
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-03-06
- Volume
- 136
- Issue
- 4
- Pages
- 1128-1138
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC3613715
- OpenAlex
- W2115298392
- Cited by
- 867
- References
- 4
- Citations by year
- 2026: 41 · 2025: 48 · 2024: 67 · 2023: 50 · 2022: 71 · 2021: 86 · 2020: 88 · 2019: 81 · 2018: 67 · 2017: 75 · 2016: 54 · 2015: 66 · 2014: 48 · 2013: 25
- FWCI
- 40.86
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Brain (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (23700433, 24500429, 23240050, 23591694)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- alpha-synuclein, prion-like spreading, synucleinopathies, dementia with Lewy bodies, Lewy bodies, Lewy neurites, alpha-synuclein fibrils, transneuronal spread, mouse model, neurodegeneration
- MeSH terms
- Administration, Intranasal, Animals, Behavior, Animal, Brain, Disease Models, Animal, Female, Humans, Injections, Intraventricular, Mice, Inbred C57BL, Prions, Recombinant Proteins, Time Factors, Lewy Body Disease, Mice, alpha-Synuclein
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