RT Conference Proceedings
T1 Decoding damage-associated microglia in post mortem hippocampus of Alzheimer’s disease patients
A1 Sánchez-Mejías, Elisabeth
A1 Mejías-Ortega, Marina
A1 Navarro, Victoria
A1 Gómez-Arboledas, Ángela
A1 Núñez-Díaz, Cristina
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 relationship between Alzheimer’s disease (AD) and neuroinflammation has become stronger since theidentification of several genetic risk factors related to microglial function. Though the role of microglial cells in the development/progression of AD is still unknown, a dysfunctional response has recently gained support. In this sense, we have reported an attenuated microglial activation associated to amyloid plaques in the hippocampus of AD patients, including a prominent degenerative process of the microglial population in the dentate gyrus, which was in contrast to the exacerbated microglial response in amyloidogenic models. This microglial degeneration could compromise their normal role of surveying the brain environment and respond to the damage. Here, we have further analyzed the phenotypic profile displayed by the damage-associated microglial cells by immunostaining and qPCR in the hippocampus of postmortem samples of AD patients (Braak V-VI) and control cases (Braak 0-II). Damage-associated microglial cells of Braak V-VI individuals were clustered around amyloid plaques and expressed Iba1, CD68, Trem2, TMEM119 and CD45high. A subset of these cells also expressed ferritin. On the contrary, these microglia down-regulated homeostatic markers, such as Cx3cr1 and P2ry12. The homeostatic and ramified microglial cells of non-demented Braak II cases were characterized by Iba1, CX3CR1, P2ry12, TMEM119 and CD45low expression. The dynamic of the microglial molecular phenotypes associated to AD pathology needs to be considered for better understand the disease complexity and, therefore, guarantee clinical success. Correcting dysregulated brain inflammatory responses might be a promising avenue to prevent/slow cognitive decline.
YR 2019
FD 2019-07-18
LK https://hdl.handle.net/10630/18082
UL https://hdl.handle.net/10630/18082
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 funds from European Union.
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 19 ene 2026