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dc.creatorGómez Oliva, Ricardoes
dc.creatorMartínez Ortega, Sergioes
dc.creatorAtienza Navarro, Isabeles
dc.creatorDomínguez García, Samueles
dc.creatorBernal Utrera, Carloses
dc.creatorGeribaldi Doldan, Noeliaes
dc.creatorVerastegui, Cristinaes
dc.creatorNúñez Abades, Pedro Antonioes
dc.creatorGarcía Alloza, Mónicaes
dc.creatorCastro, Carmenes
dc.date.accessioned2024-05-08T10:26:09Z
dc.date.available2024-05-08T10:26:09Z
dc.date.issued2023-03-19
dc.identifier.citationGómez Oliva, R., Martínez Ortega, S., Atienza Navarro, I., Domínguez García, S., Bernal Utrera, C., Geribaldi Doldan, N.,...,Castro, C. (2023). Rescue of neurogenesis and age-associated cognitive decline in SAMP8 mouse: Role of transforming growth factor-alpha. Aging Cell, 22 (6), e13829. https://doi.org/10.1111/acel.13829.
dc.identifier.issn1474-9718es
dc.identifier.issn1474-9726es
dc.identifier.urihttps://hdl.handle.net/11441/157876
dc.description.abstractNeuropathological aging is associated with memory impairment and cognitive decline, affecting several brain areas including the neurogenic niche of the dentate gyrus of the hippocampus (DG). In the healthy brain, homeostatic mechanisms regulate neuro -genesis within the DG to facilitate the continuous generation of neurons from neural stem cells (NSC). Nevertheless, aging reduces the number of activated neural stem cells and diminishes the number of newly generated neurons. Strategies that promote neurogenesis in the DG may improve cognitive performance in the elderly resulting in the development of treatments to prevent the progression of neurological disorders in the aged population. Our work is aimed at discovering targeting molecules to be used in the design of pharmacological agents that prevent the neurological effects of brain aging. We study the effect of age on hippocampal neurogenesis using the SAMP8 mouse as a model of neuropathological aging. We show that in 6- month-old SAMP8 mice, episodic and spatial memory are impaired; concomitantly, the genera -tion of neuroblasts and neurons is reduced and the generation of astrocytes is in-creased in this model. The novelty of our work resides in the fact that treatment of SAMP8 mice with a transforming growth factor- alpha (TGFα) targeting moleculeprevents the observed defects, positively regulating neurogenesis and improving cog-nitive performance. This compound facilitates the release of TGFα in vitro and in vivo and activates signaling pathways initiated by this growth factor. We conclude that compounds of this kind that stimulate neurogenesis may be useful to counteract the neurological effects of pathological agines
dc.description.sponsorshipAgencia Estatal de Investigacion RTI-2018-099908-B-C21; RTI-2018-099908-B-C22es
dc.description.sponsorshipConsejeria de Economia, Innovacion, Ciencia y Empleo, Junta de Andalucia, Fondos FEDER FEDER-UCA18-106647es
dc.description.sponsorshipConsejeria de Salud, Junta de Andalucia, FEDER fondos regionales integrados (ITI) ITI-Cadiz-0042-2019es
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherWiley Open Accesses
dc.relation.ispartofAging Cell, 22 (6), e13829.
dc.rightsAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectadult hippocampal neurogenesises
dc.subjectagines
dc.subjectdentate gyrues
dc.subjectditerpenees
dc.subjectmemoryes
dc.subjectneuroregeneratioes
dc.subject, transforming growth factor-alphaes
dc.titleRescue of neurogenesis and age-associated cognitive decline in SAMP8 mouse: Role of transforming growth factor-alphaes
dc.typeinfo:eu-repo/semantics/articlees
dc.type.versioninfo:eu-repo/semantics/publishedVersiones
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.contributor.affiliationUniversidad de Sevilla. Departamento de Fisiologíaes
dc.relation.projectIDRTI-2018-099908-B-C21es
dc.relation.projectIDRTI-2018-099908-B-C22es
dc.relation.projectIDFEDER-UCA18-106647es
dc.relation.projectIDITI-Cadiz-0042-2019es
dc.relation.publisherversionhttps://doi.org/10.1111/acel.13829es
dc.identifier.doi10.1111/acel.13829es
dc.journaltitleAging Celles
dc.publication.volumen22es
dc.publication.issue6es
dc.publication.initialPagee13829es
dc.contributor.funderAgencia Estatal de Investigación. Españaes
dc.contributor.funderEuropean Commission (EC). Fondo Europeo de Desarrollo Regional (FEDER)es
dc.contributor.funderJunta de Andalucíaes

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