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

ABSTRACT:

Objectives

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 phenotype 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.

Methods

We carried out proteomic analysis and monitored [¹⁸F]-fluoro-2-deoxy-d-glucose uptake into brain slices of Gdi1 knockout and wild type control mice. d-Glucose utilization at single astrocy

SUBMITTER: D'Adamo P 

PROVIDER: S-EPMC7871014 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature