dc.creator | Romero Molina, Carmen | es |
dc.creator | Navarro Garrido, Victoria | es |
dc.creator | Sánchez Varo, Raquel María | es |
dc.creator | Jiménez Muñoz, Sebastián | es |
dc.creator | Fernández Valenzuela, Juan José | es |
dc.creator | Sánchez Mico, María | es |
dc.creator | Muñoz Castro, Clara | es |
dc.creator | Gutiérrez Pérez, Antonia | es |
dc.creator | Vitorica Ferrández, Francisco Javier | es |
dc.creator | Vizuete Chacón, María Luisa | es |
dc.date.accessioned | 2019-01-16T13:35:08Z | |
dc.date.available | 2019-01-16T13:35:08Z | |
dc.date.issued | 2018-11-14 | |
dc.identifier.citation | Romero Molina, C., Navarro Garrido, V., Sánchez Varo, R.M., Jiménez Muñoz, S., Fernández Valenzuela, J.J., Sánchez Mico, M.,...,Vizuete Chacón, M.L. (2018). Distinct Microglial Responses in Two Transgenic Murine Models of TAU Pathology. Frontiers in Cellular Neuroscience, 12, 421. | |
dc.identifier.issn | 1662-5102 | es |
dc.identifier.uri | https://hdl.handle.net/11441/81641 | |
dc.description.abstract | Microglial cells are crucial players in the pathological process of neurodegenerative
diseases, such as Alzheimer’s disease (AD). Microglial response in AD has been
principally studied in relation to amyloid-beta pathology but, comparatively, little is known
about inflammatory processes associated to tau pathology. In the hippocampus of
AD patients, where tau pathology is more prominent than amyloid-beta pathology,
a microglial degenerative process has been reported. In this work, we have directly
compared the microglial response in two different transgenic tau mouse models:
ThyTau22 and P301S. Surprisingly, these two models showed important differences
in the microglial profile and tau pathology. Where ThyTau22 hippocampus manifested
mild microglial activation, P301S mice exhibited a strong microglial response in parallel
with high phospho-tau accumulation. This differential phospho-tau expression could
account for the different microglial response in these two tau strains. However, soluble
(S1) fractions from ThyTau22 hippocampus presented relatively high content of soluble
phospho-tau (AT8-positive) and were highly toxic for microglial cells in vitro, whereas
the correspondent S1 fractions from P301S mice displayed low soluble phosphotau
levels and were not toxic for microglial cells. Therefore, not only the expression
levels but the aggregation of phospho-tau should differ between both models. In fact,
most of tau forms in the P301S mice were aggregated and, in consequence, forming
insoluble tau species.We conclude that different factors as tau mutations, accumulation,
phosphorylation, and/or aggregation could account for the distinct microglial responses
observed in these two tau models. For this reason, deciphering the molecular nature of
toxic tau species for microglial cells might be a promising therapeutic approach in order
to restore the deficient immunological protection observed in AD hippocampus. | es |
dc.description.sponsorship | CIBERNED | es |
dc.description.sponsorship | Junta de Andalucía. Consejería de Economía, Innovación, Ciencia y Empleo CTS-2035 | es |
dc.description.sponsorship | Fundación Tatiana Pérez de Guzmán el Bueno | es |
dc.description.sponsorship | Ministerio de Ciencia, Innovación y Universidades | es |
dc.description.sponsorship | Instituto de Salud Carlos III. Fondo de Investigación Sanitaria. PI15/00957 PI15/00796 | es |
dc.description.sponsorship | Fondo Europeo de Desarrollo Regional PI15/00957 PI15/00796 | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | Frontiers Media Research Foundation | es |
dc.relation.ispartof | Frontiers in Cellular Neuroscience, 12, 421. | |
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 | TAU Models | es |
dc.subject | Inflammation | es |
dc.subject | Tauopathies | es |
dc.title | Distinct Microglial Responses in Two Transgenic Murine Models of TAU Pathology | 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.contributor.affiliation | Instituto de Biomedicina de Sevilla (IBIS) | es |
dc.relation.projectID | PI15/00957 | es |
dc.relation.projectID | PI15/00796 | es |
dc.relation.projectID | CTS-2035 | es |
dc.relation.publisherversion | https://doi.org/10.3389/fncel.2018.00421 | es |
dc.identifier.doi | 10.3389/fncel.2018.00421 | es |
idus.format.extent | 12 p. | es |
dc.journaltitle | Frontiers in Cellular Neuroscience | es |
dc.publication.volumen | 12 | es |
dc.publication.initialPage | 421-1 | es |
dc.publication.endPage | 421-12 | es |