Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/4678
DC FieldValueLanguage
dc.contributor.authorFerreiro, Elisabete-
dc.contributor.authorOliveira, Catarina R.-
dc.contributor.authorPereira, Cláudia M.F.-
dc.date.accessioned2008-09-01T14:12:35Z-
dc.date.available2008-09-01T14:12:35Z-
dc.date.issued2008en_US
dc.identifier.citationNeurobiology of Disease. 30:3 (2008) 331-342en_US
dc.identifier.urihttp://hdl.handle.net/10316/4678-
dc.description.abstractIn this study, we analyzed whether ER Ca2+ release, induced by amyloid-[beta] (A[beta]) and prion (PrP) peptides activates the mitochondrial-mediated apoptotic pathway. In cortical neurons, addition of the synthetic A[beta]1-40 or PrP106-126 peptides depletes ER Ca2+ content, leading to cytosolic Ca2+ overload. The Ca2+ released through ryanodine (RyR) and inositol 1,4,5-trisphosphate (IP3R) receptors was shown to be involved in the loss of mitochondrial membrane potential, Bax translocation to mitochondria and apoptotic death. Our data further demonstrate that Ca2+ released from the ER leads to the depletion of endogenous GSH levels and accumulation of reactive oxygen species, which were also involved in the depolarization of the mitochondrial membrane. These results illustrate that the early A[beta]- and PrP -induced perturbation of ER Ca2+ homeostasis affects mitochondrial function, activating the mitochondrial-mediated apoptotic pathway and help to clarify the mechanism implicated in neuronal death that occurs in AD and PrD.en_US
dc.description.urihttp://www.sciencedirect.com/science/article/B6WNK-4RWBSWS-2/1/e5d04335492f8e5aeee9fa1799fd3018en_US
dc.format.mimetypeaplication/PDFen
dc.language.isoengeng
dc.rightsopenAccesseng
dc.subjectAlzheimer's diseaseen_US
dc.subjectPrion disordersen_US
dc.subjectAmyloid-βen_US
dc.subjectpeptideen_US
dc.subjectPrion peptideen_US
dc.subjectApoptosisen_US
dc.subjectCa2+ homeostasisen_US
dc.subjectEndoplasmic reticulumen_US
dc.subjectMitochondriaen_US
dc.subjectOxidative stressen_US
dc.titleThe release of calcium from the endoplasmic reticulum induced by amyloid-beta and prion peptides activates the mitochondrial apoptotic pathwayen_US
dc.typearticleen_US
item.grantfulltextopen-
item.languageiso639-1en-
item.fulltextCom Texto completo-
Appears in Collections:FMUC Medicina - Artigos em Revistas Internacionais
Files in This Item:
File Description SizeFormat
filebc5e3e41b04549c8a5f99ad85f48a38a.pdf1.24 MBAdobe PDFView/Open
Show simple item record

Page view(s) 50

361
checked on Mar 23, 2020

Download(s) 20

902
checked on Mar 23, 2020

Google ScholarTM

Check


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