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

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

Oporto

Congreso; ISN-ESN 2023 Meeting; 2023

International Society for Neurochemistry

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