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dc.contributor.authorDelgado-Morales, Raúl
dc.contributor.authorAgis Balboa, Roberto Carlos 
dc.contributor.authorEsteller, Manel
dc.contributor.authorBerdasco, Maria
dc.date.accessioned2017-10-16T11:09:21Z
dc.date.available2017-10-16T11:09:21Z
dc.date.issued2017
dc.identifier.issn1868-7075
dc.identifier.otherhttps://www.ncbi.nlm.nih.gov/pubmed/28670349es
dc.identifier.otherhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5493012/es
dc.identifier.urihttp://hdl.handle.net/20.500.11940/9782
dc.description.abstractAgeing is the main risk factor for human neurological disorders. Among the diverse molecular pathways that govern ageing, epigenetics can guide age-associated decline in part by regulating gene expression and also through the modulation of genomic instability and high-order chromatin architecture. Epigenetic mechanisms are involved in the regulation of neural differentiation as well as in functional processes related to memory consolidation, learning or cognition during healthy lifespan. On the other side of the coin, many neurodegenerative diseases are associated with epigenetic dysregulation. The reversible nature of epigenetic factors and, especially, their role as mediators between the genome and the environment make them exciting candidates as therapeutic targets. Rather than providing a broad description of the pathways epigenetically deregulated in human neurological disorders, in this review, we have focused on the potential use of epigenetic enzymes as druggable targets to ameliorate neural decline during normal ageing and especially in neurological disorders. We will firstly discuss recent progress that supports a key role of epigenetic regulation during healthy ageing with an emphasis on the role of epigenetic regulation in adult neurogenesis. Then, we will focus on epigenetic alterations associated with ageing-related human disorders of the central nervous system. We will discuss examples in the context of psychiatric disorders, including schizophrenia and posttraumatic stress disorders, and also dementia or Alzheimer's disease as the most frequent neurodegenerative disease. Finally, methodological limitations and future perspectives are discussed.es
dc.description.sponsorshipEU Joint Programme-Neurodegenerative Disease Research (JPND; EPI-AD Consortium)es
dc.description.sponsorshipRecerCaixa Foundation, Federación Española de Enfermedades Raras (FEDER)es
dc.description.sponsorshipFederación Española de Enfermedades Neuromusculares (ASEM)es
dc.description.sponsorshipFundación Isabel Gemioes
dc.description.sponsorshipAsociación Española Contra el Cáncer (AECC)es
dc.description.sponsorshipMinisterio de Sanidad, Servicios Sociales e Igualdades
dc.language.isoenges
dc.rightsAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subject.meshEpigenesis, Genetic *
dc.subject.meshNeurogenesis *
dc.subject.meshDNA Methylation *
dc.titleEpigenetic mechanisms during ageing and neurogenesis as novel therapeutic avenues in human brain disorderses
dc.typeArtigoes
dc.identifier.doi10.1186/s13148-017-0365-z
dc.identifier.essn1868-7083
dc.identifier.pmid28670349
dc.issue.number1es
dc.journal.titleClinical epigeneticses
dc.organizationServizo Galego de Saúde::Estrutura de Xestión Integrada (EOXI)::EOXI de Vigo - Complexo Hospitalario Universitario de Vigo::Psiquiatríaes
dc.page.initial67es
dc.relation.projectIDRamón & Cajal (RYC-2014-15246)es
dc.relation.projectIDAxencia Galega de Innovación (GAIN) grant (IN607D-2016/003)es
dc.relation.publisherversionhttps://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1186/s13148-017-0365-zes
dc.rights.accessRightsopenAccesses
dc.subject.decsneurogénesis *
dc.subject.decsepigénesis genética *
dc.subject.decsmetilación del ADN *
dc.subject.keywordenfermedades mentaleses
dc.subject.keywordepigeneticaes
dc.subject.keywordneurodegeneraciónes
dc.typefidesArtigo Científico (inclue Orixinal, Orixinal breve, Revisión Sistemática e Meta-análisis)es
dc.typesophosArtículo Originales
dc.volume.number9es


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Atribución 4.0 Internacional
Except where otherwise noted, this item's license is described as Atribución 4.0 Internacional