Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/4738
DC FieldValueLanguage
dc.contributor.authorFerreiro, Elisabete-
dc.contributor.authorResende, Rosa-
dc.contributor.authorCosta, Rui-
dc.contributor.authorOliveira, Catarina R.-
dc.contributor.authorPereira, Cláudia M. F.-
dc.date.accessioned2008-09-01T14:13:37Z-
dc.date.available2008-09-01T14:13:37Z-
dc.date.issued2006en_US
dc.identifier.citationNeurobiology of Disease. 23:3 (2006) 669-678en_US
dc.identifier.urihttps://hdl.handle.net/10316/4738-
dc.description.abstractPrion (PrP) and amyloid-[beta] (A[beta]) peptides are involved in the neuronal loss that occurs in Prion disorders (PrD) and Alzheimer's disease (AD), respectively, partially due to Ca2+ dysregulation. Besides, the endoplasmic reticulum (ER) stress has an active role in the neurotoxic mechanisms that lead to these pathologies. Here, we analyzed whether the ER-mediated apoptotic pathway is involved in the toxic effect of synthetic PrP and A[beta] peptides. In PrP106-126- and A[beta]1-40-treated cortical neurons, the release of Ca2+ through ER ryanodine (RyR) and inositol 1,4,5-trisphosphate (IP3R) receptors induces ER stress and leads to increased cytosolic Ca2+ and reactive oxygen species (ROS) levels and subsequently to apoptotic death involving mitochondrial cytochrome c release and caspases activation. These results demonstrate that the early PrP- and A[beta]-induced perturbation of ER Ca2+ homeostasis is a death message that leads to neuronal loss, suggesting that the regulation of ER Ca2+ levels may be a potential therapeutical target for PrD and AD.en_US
dc.description.urihttp://www.sciencedirect.com/science/article/B6WNK-4KF1HJF-2/1/1c70b53c2d3ffe42c231154f0fe9258aen_US
dc.format.mimetypeaplication/PDFen
dc.language.isoengeng
dc.rightsopenAccesseng
dc.subjectPrion disordersen_US
dc.subjectAlzheimer's diseaseen_US
dc.subjectPrion peptideen_US
dc.subjectAmyloid-β peptideen_US
dc.subjectApoptosisen_US
dc.subjectCa2+ homeostasisen_US
dc.subjectEndoplasmic reticulumen_US
dc.subjectOxidative stressen_US
dc.titleAn endoplasmic-reticulum-specific apoptotic pathway is involved in prion and amyloid-beta peptides neurotoxicityen_US
dc.typearticleen_US
dc.identifier.doi10.1016/j.nbd.2006.05.011-
item.openairetypearticle-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.grantfulltextopen-
item.fulltextCom Texto completo-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.orcid0000-0002-1200-4602-
crisitem.author.orcid0000-0002-0504-5756-
crisitem.author.orcid0000-0001-6942-4328-
crisitem.author.orcid0000-0002-6630-5056-
Appears in Collections:FMUC Medicina - Artigos em Revistas Internacionais
Files in This Item:
File Description SizeFormat
fileabfe60f7eb304f3d83050c336c1d4af0.pdf529.35 kBAdobe PDFView/Open
Show simple item record

SCOPUSTM   
Citations

187
checked on Mar 25, 2024

WEB OF SCIENCETM
Citations

180
checked on Mar 2, 2024

Page view(s) 50

511
checked on Mar 26, 2024

Download(s) 20

1,034
checked on Mar 26, 2024

Google ScholarTM

Check

Altmetric

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.