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dc.contributor.authorJové Font, Mariona
dc.contributor.authorMota Martorell, Natàlia
dc.contributor.authorTorres Cabestany, Pascual
dc.contributor.authorAyala Jové, Ma. Victoria (Maria Victoria)
dc.contributor.authorPortero Otín, Manuel
dc.contributor.authorFerrer, Isidre
dc.contributor.authorPamplona Gras, Reinald
dc.date.accessioned2022-05-17T12:28:54Z
dc.date.available2022-05-17T12:28:54Z
dc.date.issued2021
dc.identifier.issn2075-1729
dc.identifier.urihttp://hdl.handle.net/10459.1/83308
dc.description.abstractCurrent shreds of evidence point to the entorhinal cortex (EC) as the origin of the Alzheimer’s disease (AD) pathology in the cerebrum. Compared with other cortical areas, the neurons from this brain region possess an inherent selective vulnerability derived from particular oxidative stress conditions that favor increased mitochondrial molecular damage with early bioenergetic involvement. This alteration of energy metabolism is the starting point for subsequent changes in a multitude of cell mechanisms, leading to neuronal dysfunction and, ultimately, cell death. These events are induced by changes that come with age, creating the substrate for the alteration of several neuronal pathways that will evolve toward neurodegeneration and, consequently, the development of AD pathology. In this context, the present review will focus on description of the biological mechanisms that confer vulnerability specifically to neurons of the entorhinal cortex, the changes induced by the aging process in this brain region, and the alterations at the mitochondrial level as the earliest mechanism for the development of AD pathology. Current findings allow us to propose the existence of an altered allostatic mechanism at the entorhinal cortex whose core is made up of mitochondrial oxidative stress, lipid metabolism, and energy production, and which, in a positive loop, evolves to neurodegeneration, laying the basis for the onset and progression of AD pathology.ca_ES
dc.description.sponsorshipResearch by the authors was supported by the Institute of Health Carlos III (FIS grantsPI14/00757, PI14/00328, PI20/0155), the Spanish Ministry of Science, Innovation, and Universities(Ministerio de Ciencia, Innovación y Universidades, grant RTI2018-099200-B-I00), and the Generalitatof Catalonia: Agency for Management of University and Research Grants (2017SGR696) to M.P-O.,I.F., and R.P. This study was co-financed by FEDER funds from the European Union (‘A way tobuild Europe’).ca_ES
dc.language.isoengca_ES
dc.publisherMDPIca_ES
dc.relationMINECO/PN2013-2016/RTI2018-099200-B-I00ca_ES
dc.relation.isformatofReproducció del document publicat a: https://doi.org/10.3390/life11050388ca_ES
dc.relation.ispartofLife, 2021, vol. 11, núm. 5ca_ES
dc.rightscc-by (c) Authors, 2021ca_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectAgingca_ES
dc.subjectATP synthaseca_ES
dc.subjectEnergy metabolismca_ES
dc.subjectEntorhinal cortexca_ES
dc.subjectLipoxidation-derived damageca_ES
dc.subjectMitochondrial dysfunctionca_ES
dc.subjectNeurodegenerationca_ES
dc.subjectOxidative damageca_ES
dc.titleThe Causal Role of Lipoxidative Damage in Mitochondrial Bioenergetic Dysfunction Linked to Alzheimer's Disease Pathologyca_ES
dc.typeinfo:eu-repo/semantics/articleca_ES
dc.identifier.idgrec031694
dc.type.versioninfo:eu-repo/semantics/publishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.3390/life11050388


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