RT Conference Proceedings
T1 Microglial responses in the human Alzheimer’s disease frontal cortex
A1 Mejías-Ortega, Marina
A1 Sánchez-Mejías, Elisabeth
A1 Navarro, Victoria
A1 Núñez-Díaz, Cristina
A1 Gómez-Arboledas, Ángela
A1 Sánchez-Varo, Raquel María
A1 Vizuete, María Luisa
A1 Dávila-Cansino, José Carlos
A1 Vitorica Ferrández, Javier
A1 Gutiérrez-Pérez, Antonia
K1 Alzheimer, Enfermedad de
K1 Microglia
AB The continuing failure to develop an effective treatment for Alzheimer’s disease (AD) reveals the complexity forthis pathology. Increasing evidence indicates that neuroinflammation involving particularly microglial cellscontributes to AD pathogenesis. The actual view, based on the findings in APP based models, gives acytotoxic/proinflammatory role to activated microglia. However, we have previously reported a limited activationand microglial degeneration in the hippocampus of AD patients in contrast with that observed in amyloidogenicmodels. Here, we evaluated the microglial response in a different region of AD brains, the frontal cortex. Postmortem tissue from controls (Braak 0-II) and AD patients (Braak V-VI) including familial cases, were obtainedfrom Spain Neurological Tissue Banks. Cellular (immunohistochemistry and image analysis) and molecular(qPCR and western blots) approaches were performed. Frontal cortex of AD patients (Braak V-VI) showedstrong microglial activation similar to that observed in amyloidogenic mice. These strongly activated microglialcells, predominantly located surrounding amyloid plaques, could drive the AD pathology and, in consequence,could be implicated in the pathology progression. Furthermore, different microglial responses were observedbetween sporadic and familial AD cases. These findings in the frontal cortex were highly in contrast to theattenuated activation and degenerative morphology displayed by microglial cells in the hippocampus of ADpatients. Regional differences in the microglial response suggest different functional states of microglial cells in aregion-specific manner. All together, these data provide a better understanding of the immunologicalmechanisms underlying AD progression and uncover new potential therapeutic targets to fight this devastatingneurodegenerative disease.
YR 2019
FD 2019-07-17
LK https://hdl.handle.net/10630/18069
UL https://hdl.handle.net/10630/18069
LA eng
NO Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.Supported by PI18/01557 (AG) and PI18/01556 (JV) grants from ISCiii of Spain co-financed by FEDER fundsfrom European Union
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 21 ene 2026