dc.creator | San Martín Rovirosa, Carol | |
dc.creator | Veloso, Pablo | |
dc.creator | Adasme, Tatiana | |
dc.creator | Lobos, Pedro | |
dc.creator | Bruna, Barbara | |
dc.creator | Galaz, Jose | |
dc.creator | García, Alejandra | |
dc.creator | Hartel, Steffen | |
dc.creator | Hidalgo Tapia, María Cecilia | |
dc.creator | Paula Lima, Andrea | |
dc.date.accessioned | 2018-12-20T14:15:26Z | |
dc.date.available | 2018-12-20T14:15:26Z | |
dc.date.created | 2018-12-20T14:15:26Z | |
dc.date.issued | 2017 | |
dc.identifier | Frontiers in Molecular Neuroscience, Volumen 10, | |
dc.identifier | 16625099 | |
dc.identifier | 10.3389/fnmol.2017.00115 | |
dc.identifier | https://repositorio.uchile.cl/handle/2250/155300 | |
dc.description.abstract | © 2017 SanMartín, Veloso, Adasme, Lobos, Bruna, Galaz, García, Hartel, Hidalgo and Paula-Lima. Amyloid β peptide oligomers (AβOs), toxic aggregates with pivotal roles in Alzheimer’s disease, trigger persistent and low magnitude Ca2+ signals in neurons. We reported previously that these Ca2+ signals, which arise from Ca2+ entry and subsequent amplification by Ca2+ release through ryanodine receptor (RyR) channels, promote mitochondrial network fragmentation and reduce RyR2 expression. Here, we examined if AβOs, by inducing redox sensitive RyR-mediated Ca2+ release, stimulate mitochondrial Ca2+ -uptake, ROS generation and mitochondrial fragmentation, and also investigated the effects of the antioxidant N-acetyl cysteine (NAC) and the mitochondrial antioxidant EUK-134 on AβOs-induced mitochondrial dysfunction. In addition, we studied the contribution of the RyR2 isoform to AβOs-induced Ca2+ release, mitochondrial Ca2+ uptake and fragmentation. We show here that inhibition of NADPH oxidase | |
dc.language | en | |
dc.publisher | Frontiers Research Foundation | |
dc.rights | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | |
dc.rights | Attribution-NonCommercial-NoDerivs 3.0 Chile | |
dc.source | Frontiers in Molecular Neuroscience | |
dc.subject | Alzheimer’s disease | |
dc.subject | Antioxidants | |
dc.subject | Endoplasmic reticulum | |
dc.subject | Mitochondrial calcium | |
dc.subject | Reactive oxygen species | |
dc.title | RyR2-mediated Ca2+ release and mitochondrial ROS generation partake in the synaptic dysfunction caused by amyloid β peptide oligomers | |
dc.type | Artículos de revistas | |