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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...
| Autores principales: | , , , , |
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| Formato: | Online Artículo Texto |
| Lenguaje: | English |
| Publicado: |
Springer Berlin Heidelberg
2016
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| Materias: | |
| Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4789229/ https://www.ncbi.nlm.nih.gov/pubmed/26820848 http://dx.doi.org/10.1007/s00401-016-1538-0 |