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                  <mods:namePart>Mejías-Ortega, Marina</mods:namePart>
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                  <mods:namePart>Sánchez-Mejías, Elisabeth</mods:namePart>
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                  <mods:namePart>Navarro, Victoria</mods:namePart>
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                  <mods:namePart>Núñez-Díaz, Cristina</mods:namePart>
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                  <mods:namePart>Jiménez, Sebastián</mods:namePart>
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                  <mods:namePart>Dávila-Cansino, José Carlos</mods:namePart>
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                  <mods:namePart>Vitorica Ferrández, Javier</mods:namePart>
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                  <mods:namePart>Gutiérrez-Pérez, Antonia</mods:namePart>
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               <mods:abstract>Microglial cells, the immune cells of the brain, and the neuroinflammatory process associated, have been&#xd;
postulated as a critical factor in AD pathogenesis, since the identification of genetic risk factors related to&#xd;
microglial function. However, the microglial role in the development/progression of AD has not been&#xd;
determined yet. In this sense, we have previously reported a limited activation and microglial degeneration in&#xd;
the hippocampus of AD patients in contrast to the proinflammatory view based on findings in amyloidogenic&#xd;
models. Here, we have further analyzed the functional/phenotypic profile displayed by microglial cells in other&#xd;
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.&#xd;
Microglia of Braak V-VI individuals were observed forming clusters and showed, both plaque&#xd;
(Iba1+/TMEM119+/P2ry12-/CD45high/Trem2+) and inter-plaque (Iba1+/ TMEM119+/P2ry12-/CD45high/Trem2-)&#xd;
microglial activation, similar that observed in amyloidogenic mice. By contrast, homeostatic and ramified&#xd;
microglial cells of non-demented Braak II cases presented Iba1+/P2ry12+/TMEM119+/CD45low/Trem2- profile.&#xd;
Furthermore, different microglial responses were observed between sporadic and familial AD cases.&#xd;
These different microglial phenotypes associated with AD pathology show the heterogeneity and complexity of&#xd;
the microglial phenotypes and suggest different functional states of these glial cells in a region-specific&#xd;
manner. These data need to be considered for better understand the immunological mechanisms underlying&#xd;
AD progression. Modulating brain inflammatory responses might be a promising avenue to prevent cognitive&#xd;
dysfunction in AD patients. ISCiii:PI18/01557(AG)-PI18/01556(JV);Junta Andalucia:UMA18-FEDERJA211(AG). All&#xd;
cofinanced by FEDER funds (European-Union).</mods:abstract>
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               <mods:subject>
                  <mods:topic>Microglia - Estudios, conferencias, ensayos, etc.</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Enfermos de Alzheimer - Estudios, conferencias, ensayos, etc.</mods:topic>
               </mods:subject>
               <mods:titleInfo>
                  <mods:title>Understanding microglial responses in the frontal cortex of alzheimer´s disease patients</mods:title>
               </mods:titleInfo>
               <mods:genre>conference output</mods:genre>
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