Evidence of impaired microglial autophagy in Alzheimer?s disease: from in vitro models to patients.

CARLOS POMILIO; GOROJOD ROXANA; ÁNGELES VINUESA; RUIDAVETS MIGUEL; JESSICA PRESA; AMAL GREGOSA; BENTIVEGNA MELISA; AGUSTINA ALAIMO; SOLEDAD PORTE ALCÓN; SEVLEVER GUSTAVO; KOTLER MÓNICA; BEAUQUIS JUAN; FLAVIA SARAVIA

Mar del Plata

Congreso; Reunión anual de la Sociedad Argentina de Investigaciones Clínicas; 2019

Sociedad Argentina de Investigaciones Clínicas

Alzheimer?s disease (AD) is a neurodegenerative disease characterized by the presence of extracellular amyloid plaques, mainly composed by Amyloid-β peptides (Aβ). Microglial activation plays a crucial role in the clearance of Aβ, and other studies suggest that microglial autophagy may also participate in this function. Our aim was to study whether microglial autophagy could be affected during AD progression, using in vivo and in vitro models. The hippocampus of aged PDAPPJ20 mice ?a validated animal model of AD? showed hyper reactive Iba1+ cells around plaques. 89% of microglial cells exhibited the lysosomal phagocytic marker CD68 in control aged mice, which is decreased to 76% in AD (p