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dc.contributor.authorFerreiro, Elisabete-
dc.contributor.authorResende, Rosa-
dc.contributor.authorCosta, Rui-
dc.contributor.authorOliveira, Catarina R.-
dc.contributor.authorPereira, Cláudia M.F.-
dc.identifier.citationNeurobiology of Disease. 23:3 (2006) 669-678en_US
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.subjectPrion disordersen_US
dc.subjectAlzheimer's diseaseen_US
dc.subjectPrion peptideen_US
dc.subjectAmyloid-β peptideen_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
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Appears in Collections:FMUC Medicina - Artigos em Revistas Internacionais
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