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dc.contributor.authorMoreno-García, Alexandra
dc.contributor.authorKun, Alejandra
dc.contributor.authorCalero, Miguel 
dc.contributor.authorCalero, Olga 
dc.date.accessioned2021-01-25T19:38:45Z
dc.date.available2021-01-25T19:38:45Z
dc.date.issued2021-01-16
dc.identifier.citationAntioxidants (Basel) . 2021 Jan 16;10(1):E124.es_ES
dc.identifier.issn2076-3921es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/11671
dc.description.abstractAging is associated with an increasing dysfunction of key brain homeostasis mechanisms and represents the main risk factor across most neurodegenerative disorders. However, the degree of dysregulation and the affectation of specific pathways set apart normal aging from neurodegenerative disorders. In particular, the neuronal metabolism of catecholaminergic neurotransmitters appears to be a specifically sensitive pathway that is affected in different neurodegenerations. In humans, catecholaminergic neurons are characterized by an age-related accumulation of neuromelanin (NM), rendering the soma of the neurons black. This intracellular NM appears to serve as a very efficient quencher for toxic molecules. However, when a neuron degenerates, NM is released together with its load (many undegraded cellular components, transition metals, lipids, xenobiotics) contributing to initiate and worsen an eventual immune response, exacerbating the oxidative stress, ultimately leading to the neurodegenerative process. This review focuses on the analysis of the role of NM in normal aging and neurodegeneration related to its capabilities as an antioxidant and scavenging of harmful molecules, versus its involvement in oxidative stress and aberrant immune response, depending on NM saturation state and its extracellular release.es_ES
dc.description.sponsorshipThis work was supported by grants SAF2016-78603-R and PID2019-110401RB-100 from the Spanish Ministry of Economy, Industry and Competitiveness (MINECO) to MC and the Spanish CIBERNED network (OC, AM-G).es_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.relation.isversionofPostprintes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectimmune responsees_ES
dc.subjectneurodegenerationes_ES
dc.subjectneuromelanin (NM)es_ES
dc.subjectoxidative stresses_ES
dc.subjectreactive oxygen species (ROS)es_ES
dc.titleThe Neuromelanin Paradox and Its Dual Role in Oxidative Stress and Neurodegeneration.es_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID33467040es_ES
dc.format.volume10es_ES
dc.format.number1es_ES
dc.identifier.doi10.3390/antiox10010124es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderCentro de Investigación Biomedica en Red - CIBERNEDes_ES
dc.description.peerreviewedSies_ES
dc.relation.publisherversionhttps://doi.org/10.3390/antiox10010124es_ES
dc.identifier.journalAntioxidants (Basel, Switzerland)es_ES
dc.repisalud.centroISCIII::Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC)es_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2016-78603-Res_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PID2019-110401RB-100es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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