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dc.contributor.authorMartín Maestro, Patricia
dc.contributor.authorGargini, Ricardo
dc.contributor.authorGarcía, Esther
dc.contributor.authorSimón, Diana
dc.contributor.authorÁvila, Jesús
dc.contributor.authorGarcía Escudero, Vega
dc.date.accessioned2021-03-03T09:38:51Z
dc.date.available2021-03-03T09:38:51Z
dc.date.issued2019
dc.identifier.issn1387-2877spa
dc.identifier.urihttp://hdl.handle.net/10641/2242
dc.description.abstractMitochondrial alterations and oxidative stress are common features of Alzheimer’s disease brain and peripheral tissues. Moreover, mitochondrial recycling process by autophagy has been found altered in the sporadic form of the disease. However, the contribution of the main proteins involved in this pathology such as amyloid- protein precursor (A PP) and tau needs to be achieved.With this aim, human unmodified fibroblasts were transduced with lentivectors encoding APP and Tau and treated with CCCP to study the mitophagy process. Both A PP and tau separately increased autophagy flux mainly by improving degradation phase. However, in the specific case of mitophagy, labeling of mitochondria by PINK1 and PARK2 to be degraded by autophagy seemed reduced, which correlates with the long-term accumulation of mitochondria. Nevertheless, the combination of tau and A PP was necessary to cause a mitophagy functional impairment reflected in the accumulation of depolarized mitochondria labeled by PINK1. The overexpression of Tau and APP recapitulates the mitophagy failure previously found in sporadic Alzheimer’s diseasespa
dc.language.isoengspa
dc.publisherJournal of Alzheimer's Diseasespa
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 España*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es/*
dc.subjectAlzheimer’s diseasespa
dc.subjectAmyloid-β protein precursorspa
dc.subjectMitochondriaspa
dc.subjectMitophagyspa
dc.titleMitophagy Failure in APP and Tau Overexpression Model of Alzheimer’s Disease.spa
dc.typearticlespa
dc.description.versionpre-printspa
dc.rights.accessRightsopenAccessspa
dc.description.extent3421 KBspa
dc.identifier.doi10.3233/JAD-190086spa
dc.relation.publisherversionhttps://content.iospress.com/articles/journal-of-alzheimers-disease/jad190086spa


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Except where otherwise noted, this item's license is described as Atribución-NoComercial-SinDerivadas 3.0 España