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GLP-1 at the Metabolic-Cognitive Interface: Reward, Affect, and Memory
Serena X Gao1,2, Léa Décarie-Spain1,3, Cindy Gu1
1Department of Biological Sciences, University of Southern California, Los Angeles, California, USA.
Comprehensive Physiology
|March 25, 2026
Summary
Glucagon-like peptide-1 (GLP-1) signaling influences cognitive functions like reward and memory. This metabolic-cognitive link impacts behaviors relevant to obesity, addiction, and mood disorders.
Area of Science:
- Neuroscience
- Endocrinology
- Metabolic Psychiatry
Background:
- Glucagon-like peptide-1 (GLP-1) is a hormone crucial for glucose homeostasis.
- GLP-1 receptors are widely distributed in the central nervous system (CNS), suggesting broader roles beyond metabolism.
- Emerging evidence links GLP-1 signaling to cognitive and affective processes.
Purpose of the Study:
- To synthesize current evidence on GLP-1 receptor (GLP-1R) signaling in cognitive functions.
- To propose a framework for GLP-1R as an interoceptive metabolic indicator.
- To explore the therapeutic potential of GLP-1R modulation for psychiatric and cognitive disorders.
Main Methods:
- Review of preclinical animal models investigating GLP-1R effects on behavior and cognition.
- Analysis of human studies examining GLP-1R agonist impacts on neural activity, mood, and cognition.
- Synthesis of data to establish a metabolic-cognitive interface framework.
Main Results:
- GLP-1R activation in animal models reduces motivation for food and drugs, modulates anxiety, and enhances learning and neuroprotection.
- Clinical studies show GLP-1R agonists alter reward cue responses and mood, with potential benefits for cognitive decline.
- Evidence suggests GLP-1R signaling links metabolic state to reward, affect, and memory.
Conclusions:
- GLP-1R signaling serves as a critical metabolic-cognitive interface.
- Understanding central GLP-1R actions is key for developing treatments for cognitive and psychiatric conditions.
- Further research is needed to differentiate direct CNS effects from indirect metabolic influences of GLP-1R interventions.
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