| Author | dc.contributor.author | Soto, Claudio | |
| Author | dc.contributor.author | Estrada, Lisbell D. | es_CL |
| Admission date | dc.date.accessioned | 2010-01-28T18:34:04Z | |
| Available date | dc.date.available | 2010-01-28T18:34:04Z | |
| Publication date | dc.date.issued | 2008-02 | |
| Cita de ítem | dc.identifier.citation | Arch Neurol.;65(2):184-189. | en_US |
| Identifier | dc.identifier.issn | SSN (printed): 0003-9942. ISSN (electronic): 0375-8540 | |
| Identifier | dc.identifier.uri | https://repositorio.uchile.cl/handle/2250/119006 | |
| Abstract | dc.description.abstract | Akey molecular pathway implicated in diverse neurodegenerative diseases is the misfolding,
aggregation, and accumulation of proteins in the brain. Compelling evidence
strongly supports the hypothesis that accumulation of misfolded proteins leads to synaptic
dysfunction, neuronal apoptosis, brain damage, and disease. However, the mechanism
by which protein misfolding and aggregation trigger neurodegeneration and the identity of
the neurotoxic structure is still unclear. The aim of this article is to review the literature around
the molecular mechanism and role of misfolded protein aggregates in neurodegeneration and the
potential for the misfolding process to lead to a transmissible form of disease by a prion-based model
of propagation. | en_US |
| Lenguage | dc.language.iso | en | en_US |
| Publisher | dc.publisher | American Medical Association | en_US |
| Título | dc.title | Protein Misfolding and Neurodegeneration | en_US |
| Document type | dc.type | Artículo de revista | |
