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dc.contributor.authorSánchez-Varo, Raquel María 
dc.contributor.authorFernández-Valenzuela, Juan José
dc.contributor.authorRomero-Molina, Carmen
dc.contributor.authorSánchez-Mejías, Elisabeth 
dc.contributor.authorGómez-Arboledas, Ángela
dc.contributor.authorNúñez-Díaz, Cristina
dc.contributor.authorNavarro, Victoria
dc.contributor.authorDávila-Cansino, José Carlos 
dc.contributor.authorVitorica Ferrández, Javier
dc.contributor.authorGutiérrez-Pérez, Antonia 
dc.date.accessioned2019-07-19T07:53:37Z
dc.date.available2019-07-19T07:53:37Z
dc.date.created2019
dc.date.issued2019-07-19
dc.identifier.urihttps://hdl.handle.net/10630/18089
dc.description.abstractAmyloid-beta (Abeta) peptide deposits and hyperphosphorylated tau protein (phospho-tau) accumulate in Alzheimer’s disease (AD) brains. These abnormal protein aggregates leads to glial activation, synaptic dysfunction, neuronal loss and cognitive decline. While microglial response has mostly been analyzed in relation to Abeta accumulation, little is still known about inflammatory processes associated with tau pathology. Microglial reactivity and defective glial responses have been involved in these proteinopathies. Our aim is to clarify the effects of Abeta and tau separately, in order to improve the comprehension of their differential contribution to neuroinflammation and neurodegeneration. We compared the progression of these processes in an amyloidogenic AD model (APPSL/PS1M146L) and two different models of tauopathy (ThyTau22 and hP301S) from 2 to 18 months of age. Accumulation of aggregated proteins was assessed using specific anti- Abeta and phospho-tau antibodies. Inflammatory response was studied using a battery of microglial markers (Iba1, CD45, CD68, Trem2 and Gal-3). In the hippocampus of these models, Tau and Abeta pathologies initiated as early as 2 months of age and increased progressively with aging. Neuritic plaques induced a strong microglial activation associated to plaques in APP/PS1 mice. Interestingly, inflammatory markers and microglial reactivity were barely increased in the hippocampus of ThyTau mice in contrast to not only APP/PS1, but also to P301S mice, which displayed a prominent microglial response. Deciphering the specific effects of Abeta, tau and their different toxic species, would indeed enable the development of novel therapeutic strategies and drugs targeting neuroinflammatory pathways related to these proteinopathies.en_US
dc.description.sponsorshipUniversidad de Málaga. Campus de excelencia Andalucía-Tech. Supported by PI18/01557 (AG) and PI18/01556 (JV) grants from ISCiii of Spain co-financed by FEDER funds from European Union, and by grant PPIT.UMA.B1.2017/26 (RS-V).en_US
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCélulas glialesen_US
dc.subjectBilología celularen_US
dc.subjectGenéticaen_US
dc.subjectFisiologíaen_US
dc.titleDissecting the microglial response in transgenic models of amyloidogenesis and tauopathyen_US
dc.typeinfo:eu-repo/semantics/conferenceObjecten_US
dc.centroFacultad de Cienciasen_US
dc.relation.eventtitleXIV European Meeting on Glial Cells in Heath and Diseaseen_US
dc.relation.eventplaceOportoen_US
dc.relation.eventdate07/2019en_US


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