P53 orchestrates the microglial response upon amyloid-beta-induced neurodegeneration in vivo

Trabajo presentado al 15th International Conference AD/PD 2021 celebrada de forma virtual del 9 al 14 de marzo de 2021Amyloid-β (Aβ) oligomers trigger signalling cascades involving alteration of calcium homeostasis, ROS production, inflammatory processes and mitochondrial dysfunction, culminating in neuronal apoptosis. According to a functional scale, microglia can be categorized into the classical pro-inflammatory/neurotoxic phenotype, known as M1, and an alternative anti-inflammatory/neuroprotective M2 phenotype, which is involved in the resolution of inflammation, phagocytosis and tissue repair. Previously, we described a key role of p53 in neurodegeneration induced by Aβ neurotoxicity in vivo. Recently, p53 has emerged as a key modulator of the immune response in microglia. Here we evaluated whether p53 is modulating the microglial response to Aβ25-35 oligomers leading to neurodegenerationFunded by The Instituto de Salud Carlos III (PI18/00265); European Union’s Horizon 2020 Research and Innovation Programme (Grant Agreement 686009) and Programa Operativo FSE Castilla y León 2014-2020