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dc.contributor.authorMejias-Ortega, Marina
dc.contributor.authorSanchez-Mejias, Elisabet
dc.contributor.authorNavarro, Victoria
dc.contributor.authorNuñez-Diaz, Cristina
dc.contributor.authorSanchez-Varo, Raquel
dc.contributor.authorJimenez, Sebastian
dc.contributor.authorDavila, Jose Carlos 
dc.contributor.authorVitorica, Javier
dc.contributor.authorGutierrez-Perez, Antonia 
dc.date.accessioned2021-03-22T09:36:29Z
dc.date.available2021-03-22T09:36:29Z
dc.date.issued2021-03-09
dc.identifier.urihttps://hdl.handle.net/10630/21223
dc.description.abstractMicroglial cells, the immune cells of the brain, and the neuroinflammatory process associated, have been postulated as a critical factor in AD pathogenesis, since the identification of genetic risk factors related to microglial function. However, the microglial role in the development/progression of AD has not been determined yet. In this sense, we have previously reported a limited activation and microglial degeneration in the hippocampus of AD patients in contrast to the proinflammatory view based on findings in amyloidogenic models. Here, we have further analyzed the functional/phenotypic profile displayed by microglial cells in other vulnerable brain region of AD patients, the frontal cortex. Immunohistochemistry and image analysis approaches were performed in the frontal cortex of post mortem samples from controls (Braak 0-II) and AD patients (Braak V-VI) including familial cases. Microglia of Braak V-VI individuals were observed forming clusters and showed, both plaque (Iba1+/TMEM119+/P2ry12-/CD45high/Trem2+) and inter-plaque (Iba1+/ TMEM119+/P2ry12-/CD45high/Trem2-) microglial activation, similar that observed in amyloidogenic mice. By contrast, homeostatic and ramified microglial cells of non-demented Braak II cases presented Iba1+/P2ry12+/TMEM119+/CD45low/Trem2- profile. Furthermore, different microglial responses were observed between sporadic and familial AD cases. These different microglial phenotypes associated with AD pathology show the heterogeneity and complexity of the microglial phenotypes and suggest different functional states of these glial cells in a region-specific manner. These data need to be considered for better understand the immunological mechanisms underlying AD progression. Modulating brain inflammatory responses might be a promising avenue to prevent cognitive dysfunction in AD patients. ISCiii:PI18/01557(AG)-PI18/01556(JV);Junta Andalucia:UMA18-FEDERJA211(AG). All cofinanced by FEDER funds (European-Union).es_ES
dc.description.sponsorshipUniversidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.es_ES
dc.language.isoenges_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.subjectMicroglia - Estudios, conferencias, ensayos, etc.es_ES
dc.subjectEnfermos de Alzheimer - Estudios, conferencias, ensayos, etc.es_ES
dc.subject.otherAlzheimeres_ES
dc.subject.otherNeuroinflammationes_ES
dc.titleUnderstanding microglial responses in the frontal cortex of alzheimer´s disease patientses_ES
dc.typeinfo:eu-repo/semantics/conferenceObjectes_ES
dc.centroFacultad de Cienciases_ES
dc.relation.eventtitleAD/PD™ 2021, Alzheimer's & Parkinson's Diseases Conferencees_ES
dc.relation.eventplaceVirtual (Barcelona)es_ES
dc.relation.eventdate09/03/2021-14/03/2021es_ES


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