Reactive astrocytes present deficits in energy metabolism and insulin signaling in an experimental model of Alzheimer's Disease

MELISA BENTIVEGNA; AMAL GREGOSA; DAIANA VOTA; CARLOS POMILIO; ÁNGELES VINUESA; NICOLÁS GONZÁLEZ PÉREZ; JESSICA PRESA; MELINA BELLOTTO; FLAVIA SARAVIA; JUAN BEAUQUIS

Congreso; Reunión bienal ISN-ESN 2023 (International Society of Neurochemistry (ISN) y la European Society of Neurochemistry (ESN)); 2023

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease and the leading cause of dementia. Besides amyloid beta (Aβ) and tau accumulation, inflammation and insulin resistance are common findings in AD brains. Astrocytes regulate these processes, maintaining brain homeostasis and coordinating the inflammatory response. In the present work, our objectives were 1) to study the metabolic and inflammatory status of the PDAPP-J20 transgenic (TG) mouse, model of AD, and 2) to evaluate astroglial activation, energy metabolism and insulin signaling upon Aβ exposure. We hypothesized that in AD, astrocytes adopt a phenotype that promotes inflammation and lose homeostatic functions. Insulin signaling measured by the pAkt/Akt ratio was impaired in the hippocampus (p