Inhibiting glycolysis rescues memory impairment in an intellectual disability Gdi1-null mouse

GDI1 gene encodes for αGDI, a protein controlling the cycling of small GTPases, reputed to orchestrate vesicle trafficking. Mutations in human GDI1 are responsible for intellectual disability (ID). In mice with ablated Gdi1, a model of ID, impaired working and associative short-term memory was recorded. This cognitive p henotype worsens if the deletion of αGDI expression is restricted to neurons. However, whether astrocytes, key homeostasis providing neuroglial cells, supporting neurons via aerobic glycolysis, contribute to this cognitive impairment is unclear.

Source: Metabolism - Clinical and Experimental - December 9, 2020 Category: Biomedical Science Authors: Patrizia D ’Adamo, Anemari Horvat, Antonia Gurgone, Maria Lidia Mignogna, Veronica Bianchi, Michela Masetti, Maddalena Ripamonti, Stefano Taverna, Jelena Velebit, Maja Malnar, Marko Muhič, Katja Fink, Angela Bachi, Umberto Restuccia, Sara Belloli, Rosa Source Type: research