dc.creator | Navarro Garrido, Victoria | es |
dc.creator | Sánchez Mejías, Elisabeth | es |
dc.creator | Jiménez Muñoz, Sebastián | es |
dc.creator | Muñoz Castro, Clara | es |
dc.creator | Sánchez Varo, Raquel María | es |
dc.creator | Dávila, José Carlos | es |
dc.creator | Vizuete Chacón, María Luisa | es |
dc.creator | Gutiérrez, Antonia | es |
dc.creator | Vitorica Ferrández, Francisco Javier | es |
dc.date.accessioned | 2018-09-25T10:24:49Z | |
dc.date.available | 2018-09-25T10:24:49Z | |
dc.date.issued | 2018 | |
dc.identifier.citation | Navarro 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.issn | 1663-4365 | es |
dc.identifier.uri | https://hdl.handle.net/11441/78800 | |
dc.description.abstract | Microglial 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.sponsorship | España, Instituto de Salud Carlos III PI15/00957, PI15/00796 | es |
dc.description.sponsorship | España Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucia Proyecto de Excelencia CTS-2035 | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | Frontiers Media | es |
dc.relation.ispartof | Frontiers in Aging Neuroscience, 10 (140), 1-8. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Alzheimer disease | es |
dc.subject | microglia | es |
dc.subject | APP models | es |
dc.subject | inflamation | es |
dc.subject | Abeta plaques | es |
dc.title | Microglia in Alzheimer’s Disease: Activated, Dysfunctional or Degenerative | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Bioquímica y Biología Molecular | es |
dc.relation.projectID | PI15/00957 | es |
dc.relation.projectID | PI15/00796 | es |
dc.relation.projectID | CTS-2035 | es |
dc.relation.publisherversion | http://dx.doi.org/10.3389/fnagi.2018.00140 | es |
dc.identifier.doi | 10.3389/fnagi.2018.00140 | es |
dc.contributor.group | Universidad de Sevilla. CTS257: Envejecimiento y Neurodegeneración | es |
idus.format.extent | 8 p. | es |
dc.journaltitle | Frontiers in Aging Neuroscience | es |
dc.publication.volumen | 10 | es |
dc.publication.issue | 140 | es |
dc.publication.initialPage | 1 | es |
dc.publication.endPage | 8 | es |
dc.contributor.funder | Instituto de Salud Carlos III | |
dc.contributor.funder | Junta de Andalucía | |