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

BENTIVEGNA M; GREGOSA A; VOTA D; POMILIO C; VINUESA A; GONZALEZ PEREZ N; PRESA J; BELLOTTO M; SARAVIA F; BEAUQUIS J

Mar del Plata

Congreso; REUNIÓN CONJUNTA SAIC SAB AAFE AACYTAL 2023; 2023

Sociedad Argentina de Investigación Clínica (SAIC)

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