Prion-like spreading of pathological α-synuclein in brain
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ID: 305506
2013
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Abstract
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.
| Reference Key |
openalex_W2115298392
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| Authors | Masami Masuda‐Suzukake, Takashi Nonaka, Masato Hosokawa, Takayuki Oikawa, Tetsuaki Arai, Haruhiko Akiyama, David Mann, Masato Hasegawa |
| Journal | Brain research |
| Year | 2013 |
| DOI |
10.1093/brain/awt037
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| URL | |
| Keywords | Keywords not found |
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