RT Conference Proceedings
T1 Understanding microglial responses in the frontal cortex of alzheimer´s disease patients
A1 Mejías-Ortega, Marina
A1 Sánchez-Mejías, Elisabeth
A1 Navarro, Victoria
A1 Núñez-Díaz, Cristina
A1 Sánchez-Varo, Raquel María
A1 Jiménez, Sebastián
A1 Dávila-Cansino, José Carlos
A1 Vitorica Ferrández, Javier
A1 Gutiérrez-Pérez, Antonia
K1 Microglia - Estudios, conferencias, ensayos, etc.
K1 Enfermos de Alzheimer - Estudios, conferencias, ensayos, etc.
AB Microglial cells, the immune cells of the brain, and the neuroinflammatory process associated, have beenpostulated as a critical factor in AD pathogenesis, since the identification of genetic risk factors related tomicroglial function. However, the microglial role in the development/progression of AD has not beendetermined yet. In this sense, we have previously reported a limited activation and microglial degeneration inthe hippocampus of AD patients in contrast to the proinflammatory view based on findings in amyloidogenicmodels. Here, we have further analyzed the functional/phenotypic profile displayed by microglial cells in othervulnerable 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 ramifiedmicroglial 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 ofthe microglial phenotypes and suggest different functional states of these glial cells in a region-specificmanner. These data need to be considered for better understand the immunological mechanisms underlyingAD progression. Modulating brain inflammatory responses might be a promising avenue to prevent cognitivedysfunction in AD patients. ISCiii:PI18/01557(AG)-PI18/01556(JV);Junta Andalucia:UMA18-FEDERJA211(AG). Allcofinanced by FEDER funds (European-Union).
YR 2021
FD 2021-03-09
LK https://hdl.handle.net/10630/21223
UL https://hdl.handle.net/10630/21223
LA eng
NO Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 24 ene 2026