Please use this identifier to cite or link to this item:
http://hdl.handle.net/2445/141852
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Río Fernández, José Antonio del | - |
dc.contributor.author | Ferrer, Isidro (Ferrer Abizanda) | - |
dc.contributor.author | Gavín Marín, Rosalina | - |
dc.date.accessioned | 2019-10-08T17:04:24Z | - |
dc.date.available | 2019-12-01T06:10:16Z | - |
dc.date.issued | 2018-06-01 | - |
dc.identifier.issn | 0301-0082 | - |
dc.identifier.uri | http://hdl.handle.net/2445/141852 | - |
dc.description.abstract | Several studies have indicated that certain misfolded amyloids composed of tau, β-amyloid or α-synuclein can be transferred from cell to cell, suggesting the contribution of mechanisms reminiscent of those by which infective prions spread through the brain. This process of a 'prion-like' spreading between cells is also relevant as a novel putative therapeutic target that could block the spreading of proteinaceous aggregates throughout the brain which may underlie the progressive nature of neurodegenerative diseases. The relevance of β-amyloid oligomers and cellular prion protein (PrPC) binding has been a focus of interest in Alzheimer's disease (AD). At the molecular level, β-amyloid/PrPC interaction takes place in two differently charged clusters of PrPC. In addition to β-amyloid, participation of PrPC in α-synuclein binding and brain spreading also appears to be relevant in α-synucleopathies. This review summarizes current knowledge about PrPC as a putative receptor for amyloid proteins and the physiological consequences of these interactions. | - |
dc.format.extent | 16 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Elsevier Ltd | - |
dc.relation.isformatof | Versió postprint del document publicat a: https://doi.org/10.1016/j.pneurobio.2018.03.001 | - |
dc.relation.ispartof | Progress in Neurobiology, 2018, vol. 165-167, p. 87-102 | - |
dc.relation.uri | https://doi.org/10.1016/j.pneurobio.2018.03.001 | - |
dc.rights | cc-by-nc-nd (c) Elsevier Ltd, 2018 | - |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/es | - |
dc.source | Articles publicats en revistes (Patologia i Terapèutica Experimental) | - |
dc.subject.classification | Amiloïdosi | - |
dc.subject.classification | Pèptids | - |
dc.subject.classification | Metabolisme | - |
dc.subject.classification | Alfa-sinucleïna | - |
dc.subject.classification | Proteïnes | - |
dc.subject.other | Amyloidosis | - |
dc.subject.other | Peptides | - |
dc.subject.other | Metabolism | - |
dc.subject.other | Alpha-synuclein | - |
dc.subject.other | Proteins | - |
dc.title | Role of cellular prion protein in interneuronal amyloid transmission | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/acceptedVersion | - |
dc.identifier.idgrec | 679823 | - |
dc.date.updated | 2019-10-08T17:04:24Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 29530723 | - |
Appears in Collections: | Articles publicats en revistes (Institut de Bioenginyeria de Catalunya (IBEC)) Articles publicats en revistes (Patologia i Terapèutica Experimental) Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
679823.pdf | 1.57 MB | Adobe PDF | View/Open |
This item is licensed under a Creative Commons License