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Axonal transport and secretion of fibrillar forms of α-synuclein, Aβ42 peptide and HTTExon 1
Accruing evidence suggests that prion-like behavior of fibrillar forms of α-synuclein, β-amyloid peptide and mutant huntingtin are responsible for the spread of the lesions that characterize Parkinson disease, Alzheimer disease and Huntington disease, respectively. It is unknown whether these distin...
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| Pubblicato in: | Acta Neuropathol |
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| Autori principali: | , , , , |
| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
Springer Berlin Heidelberg
2016
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| Soggetti: | |
| Accesso online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4789229/ https://ncbi.nlm.nih.gov/pubmed/26820848 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1007/s00401-016-1538-0 |
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