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    Por favor, use este identificador para citar o enlazar este ítem:http://uvadoc.uva.es/handle/10324/45069

    Título
    Mitochondrial Ca2+ overload underlies Aβ oligomers neurotoxicity providing an unexpected mechanism of neuroprotection by NSAIDs
    Autor
    Sanz Blasco, Sara
    Valero, Ruth Ana
    Rodríguez Crespo, Ignacio
    Villalobos Jorge, Carlos
    Núñez Llorente, LucíaAutoridad UVA
    Año del Documento
    2008
    Editorial
    Public Library of Science
    Descripción
    Producción Científica
    Documento Fuente
    PLoS ONE, 2008, vol. 3, n. 7. 16 p.
    Resumo
    Dysregulation of intracellular Ca2+ homeostasis may underlie amyloid β peptide (Aβ) toxicity in Alzheimer's Disease (AD) but the mechanism is unknown. In search for this mechanism we found that Aβ1–42 oligomers, the assembly state correlating best with cognitive decline in AD, but not Aβ fibrils, induce a massive entry of Ca2+ in neurons and promote mitochondrial Ca2+ overload as shown by bioluminescence imaging of targeted aequorin in individual neurons. Aβ oligomers induce also mitochondrial permeability transition, cytochrome c release, apoptosis and cell death. Mitochondrial depolarization prevents mitochondrial Ca2+ overload, cytochrome c release and cell death. In addition, we found that a series of non-steroidal anti-inflammatory drugs (NSAIDs) including salicylate, sulindac sulfide, indomethacin, ibuprofen and R-flurbiprofen depolarize mitochondria and inhibit mitochondrial Ca2+ overload, cytochrome c release and cell death induced by Aβ oligomers. Our results indicate that i) mitochondrial Ca2+ overload underlies the neurotoxicity induced by Aβ oligomers and ii) inhibition of mitochondrial Ca2+ overload provides a novel mechanism of neuroprotection by NSAIDs against Aβ oligomers and AD.
    Palabras Clave
    Calcium
    Calcio
    Amyloid-β oligomers
    Oligómeros β-amiloides
    Neurotoxicity
    Neurotoxicidad
    Neuroprotection
    Neuroprotección
    ISSN
    1932-6203
    Revisión por pares
    SI
    DOI
    10.1371/journal.pone.0002718
    Patrocinador
    Instituto de Salud Carlos III (grants PI04/1510 and PI07/0766)
    Junta de Castilla y León (grant VA022A05)
    Ministerio de Ciencia, Innovación y Universidades (grant BFU2006-05202)
    Version del Editor
    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0002718
    Propietario de los Derechos
    © 2008 Public Library of Science
    Idioma
    eng
    URI
    http://uvadoc.uva.es/handle/10324/45069
    Tipo de versión
    info:eu-repo/semantics/publishedVersion
    Derechos
    openAccess
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    • CFC - Artículos de Revista [38]
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    Universidad de Valladolid

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