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dc.creatorNavarro Garrido, Victoriaes
dc.creatorSánchez Mejías, Elisabethes
dc.creatorJiménez Muñoz, Sebastiánes
dc.creatorMuñoz Castro, Claraes
dc.creatorSánchez Varo, Raquel Maríaes
dc.creatorDávila, José Carloses
dc.creatorVizuete Chacón, María Luisaes
dc.creatorGutiérrez, Antoniaes
dc.creatorVitorica Ferrández, Francisco Javieres
dc.date.accessioned2018-09-25T10:24:49Z
dc.date.available2018-09-25T10:24:49Z
dc.date.issued2018
dc.identifier.citationNavarro Garrido, V., Sánchez Mejías, ., Jiménez Muñoz, S., Muñoz Castro, ., Sánchez Varo, R.M., Dávila, J.C.,...,Vizuete Chacón, M.L. (2018). Microglia in Alzheimer’s Disease: Activated, Dysfunctional or Degenerative. Frontiers in Aging Neuroscience, 10 (140), 1-8.
dc.identifier.issn1663-4365es
dc.identifier.urihttps://hdl.handle.net/11441/78800
dc.description.abstractMicroglial activation has been considered a crucial player in the pathological process of multiple human neurodegenerative diseases. In some of these pathologies, such as Amyotrophic Lateral Sclerosis or Multiple Sclerosis, the immune system and microglial cells (as part of the cerebral immunity) play a central role. In other degenerative processes, such as Alzheimer’s disease (AD), the role of microglia is far to be elucidated. In this “mini-review” article, we briefly highlight our recent data comparing the microglial response between amyloidogenic transgenic models, such as APP/PS1 and AD patients. Since the AD pathology could display regional heterogeneity, we focus our work at the hippocampal formation. In APP based models a prominent microglial response is triggered around amyloid-beta (Aβ) plaques. These strongly activated microglial cells could drive the AD pathology and, in consequence, could be implicated in the neurodegenerative process observed in models. On the contrary, the microglial response in human samples is, at least, partial or attenuated. This patent difference could simply reflect the lower and probably slower Aβ production observed in human hippocampal samples, in comparison with models, or could reflect the consequence of a chronic long-standing microglial activation. Beside this differential response, we also observed microglial degeneration in Braak V–VI individuals that, indeed, could compromise their normal role of surveying the brain environment and respond to the damage. This microglial degeneration, particularly relevant at the dentate gyrus, might be mediated by the accumulation of toxic soluble phospho-tau species. The consequences of this probably deficient immunological protection, observed in AD patients, are unknown.es
dc.description.sponsorshipEspaña, Instituto de Salud Carlos III PI15/00957, PI15/00796es
dc.description.sponsorshipEspaña Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucia Proyecto de Excelencia CTS-2035es
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherFrontiers Mediaes
dc.relation.ispartofFrontiers in Aging Neuroscience, 10 (140), 1-8.
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectAlzheimer diseasees
dc.subjectmicrogliaes
dc.subjectAPP modelses
dc.subjectinflamationes
dc.subjectAbeta plaqueses
dc.titleMicroglia in Alzheimer’s Disease: Activated, Dysfunctional or Degenerativees
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 Bioquímica y Biología Moleculares
dc.relation.projectIDPI15/00957es
dc.relation.projectIDPI15/00796es
dc.relation.projectIDCTS-2035es
dc.relation.publisherversionhttp://dx.doi.org/10.3389/fnagi.2018.00140es
dc.identifier.doi10.3389/fnagi.2018.00140es
dc.contributor.groupUniversidad de Sevilla. CTS257: Envejecimiento y Neurodegeneraciónes
idus.format.extent8 p.es
dc.journaltitleFrontiers in Aging Neurosciencees
dc.publication.volumen10es
dc.publication.issue140es
dc.publication.initialPage1es
dc.publication.endPage8es
dc.contributor.funderInstituto de Salud Carlos III
dc.contributor.funderJunta de Andalucía

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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Except where otherwise noted, this item's license is described as: Attribution-NonCommercial-NoDerivatives 4.0 Internacional