OGT Ameliorates Diabetes‐Associated Cognitive Decline via Modulation of DRP1 Function and Mitochondrial Homeostasis | Synapse
April 16, 2026
OGT Ameliorates Diabetes‐Associated Cognitive Decline via Modulation of DRP1 Function and Mitochondrial Homeostasis
Key Points
The aim is to explore how OGT deficiency affects cognitive decline related to diabetes and evaluate semaglutide as a treatment.
Evaluation of OGT deficiency and its impact on mitochondrial function.
Assessment of cognitive performance related to diabetes.
Analysis of semaglutide's effect on mitochondrial homeostasis and cognitive outcomes.
OGT deficiency leads to imbalanced mitochondrial function contributing to cognitive decline.
Semaglutide shows potential in protective effects on OGT functions.
Modulation of DRP1 activity is linked to improved cognitive health.
Abstract
OGT deficiency-mediated mitochondrial homeostasis imbalance contributes to the occurrence of DACD, and semaglutide with an OGT protective effect may be a potential therapeutic approach for DACD.