Show simple item record

Authordc.contributor.authorCornejo, Víctor Hugo 
Authordc.contributor.authorHetz Flores, Claudio es_CL
Admission datedc.date.accessioned2014-01-30T14:30:45Z
Available datedc.date.available2014-01-30T14:30:45Z
Publication datedc.date.issued2013
Cita de ítemdc.identifier.citationSemin Immunopathol (2013) 35:277–292en_US
Identifierdc.identifier.otherDOI 10.1007/s00281-013-0373-9
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/129223
General notedc.descriptionArtículo de publicación ISIen_US
Abstractdc.description.abstractAlzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by synaptic dysfunction and accumulation of amyloid-beta (Aβ) peptide, which are responsible for the progressive loss of memory. The mechanisms involved in neuron dysfunction in AD remain poorly understood. Recent evidence implicates the participation of adaptive responses to stress within the endoplasmic reticulum (ER) in the disease process, via a pathway known as the unfolded protein response (UPR). Here, we review the findings suggesting a functional role of ER stress in the etiology of AD. Possible therapeutic strategies to mitigate ER stress in the context of AD are discussed.en_US
Lenguagedc.language.isoenen_US
Publisherdc.publisherSpringeren_US
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Keywordsdc.subjectAlzheimer’s diseaseen_US
Títulodc.titleThe unfolded protein response in Alzheimer’s diseaseen_US
Document typedc.typeArtículo de revista


Files in this item

Icon

This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile