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Clinical trials that successfully reduce these abnormal protein deposits have demonstrated only modest disease-modifying effects (6, 7) highlighting the continued need for additional therapeutic approaches to prevent, slow and treat AD

In FoB, we found that ATP levels in Gclc -deficient, but not in Gclc -sufficient FoB dropped in a dose-dependent fashion in response to inhibition of glycolysis with 2-deoxy-D-glucose (2-DG) or galactose (Fig

doi: 10.3389/fragi.2022.929474 30 PellerinLMagistrettiPJ