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Distinct Microglial Responses in Two Transgenic Murine Models of TAU Pathology

 

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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, 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, 421-1-421-12.
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, 421-1-421-12.
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
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
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