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dc.contributor.authorNavarro-Lobato, Irene
dc.contributor.authorMasmudi-Martín, Mariam
dc.contributor.authorLópez-Aranda, Manuel Francisco
dc.contributor.authorLópez-Téllez, Juan Félix
dc.contributor.authorDelgado, Gloria
dc.contributor.authorGranados-Durán, Pablo
dc.contributor.authorGaona-Romero, Celia
dc.contributor.authorCarretero-Rey, Marta
dc.contributor.authorPosadas, Sinforiano
dc.contributor.authorQuirós-Ortega, María Elena
dc.contributor.authorKhan, Zafaruddin 
dc.date.accessioned2024-11-27T13:13:18Z
dc.date.available2024-11-27T13:13:18Z
dc.date.issued2023-11-08
dc.identifier.citationNavarro-Lobato I, Masmudi-Martín M, López-Aranda MF, et al. Promotion of structural plasticity in area V2 of visual cortex prevents against object recognition memory deficits in aging and Alzheimer's disease rodents. Neural Regen Res. 2024;19(8):1835-1841. doi:10.4103/1673-5374.389301es_ES
dc.identifier.urihttps://hdl.handle.net/10630/35360
dc.description.abstractMemory deficit, which is often associated with aging and many psychiatric, neurological, and neurodegenerative diseases, has been a challenging issue for treatment. Up till now, all potential drug candidates have failed to produce satisfactory effects. Therefore, in the search for a solution, we found that a treatment with the gene corresponding to the RGS14414 protein in visual area V2, a brain area connected with brain circuits of the ventral stream and the medial temporal lobe, which is crucial for object recognition memory (ORM), can induce enhancement of ORM. In this study, we demonstrated that the same treatment with RGS14414 in visual area V2, which is relatively unaffected in neurodegenerative diseases such as Alzheimer's disease, produced long-lasting enhancement of ORM in young animals and prevent ORM deficits in rodent models of aging and Alzheimer's disease. Furthermore, we found that the prevention of memory deficits was mediated through the upregulation of neuronal arborization and spine density, as well as an increase in brain-derived neurotrophic factor (BDNF). A knockdown of BDNF gene in RGS14414-treated aging rats and Alzheimer's disease model mice caused complete loss in the upregulation of neuronal structural plasticity and in the prevention of ORM deficits. These findings suggest that BDNF-mediated neuronal structural plasticity in area V2 is crucial in the prevention of memory deficits in RGS14414-treated rodent models of aging and Alzheimer's disease. Therefore, our findings of RGS14414 gene-mediated activation of neuronal circuits in visual area V2 have therapeutic relevance in the treatment of memory deficits.es_ES
dc.description.sponsorshipThis study was supported by grants from the Ministerio de Economía y Competitividad (BFU2013-43458-R) and Junta de Andalucía (P12-CTS-1694 and Proyexcel-00422) to Zafaruddin Khan.es_ES
dc.language.isoenges_ES
dc.publisherWolters Kluwer Medknowes_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectMemoria - Trastornoses_ES
dc.subjectNeuroplasticidades_ES
dc.subjectAlzheimer, Enfermedad dees_ES
dc.subjectEnvejecimientoes_ES
dc.subjectModelos animales en investigaciónes_ES
dc.subject.otherBehavioral performancees_ES
dc.subject.otherBrain-derived neurotrophic factores_ES
dc.subject.otherCognitive dysfunctiones_ES
dc.subject.otherEpisodic memoryes_ES
dc.subject.otherMemory circuit activationes_ES
dc.subject.otherMemory deficitses_ES
dc.subject.otherMemory enhancementes_ES
dc.subject.otherObject recognition memoryes_ES
dc.subject.otherPrevention of memory losses_ES
dc.subject.otherRegulator of G protein signalinges_ES
dc.titlePromotion of structural plasticity in area V2 of visual cortex prevents against object recognition memory deficits in aging and Alzheimer's disease rodents.es_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.centroFacultad de Cienciases_ES
dc.identifier.doi10.4103/1673-5374.389301
dc.rights.ccAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones_ES


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