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Glucagon-like peptide-1 (GLP-1) and glucose metabolism in human myocytes

Pain Processing Mechanisms Central Sensitization (via mGlu2 receptor upregulation)[4][5] Neuroinflammation (modulates glial activation)[12][13] Mitochondrial Dysfunction (enhances ATP production, -oxidation)[2][13] Oxidative Stress (direct antioxidant activity)[2][13] Systemic Inflammation limited direct evidence SUMMARY OVERVIEW CLINICAL PEARLS 1

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In experimental models, they preserved dopaminergic neurons and improved motor performance via mitochondrial and endoplasmic reticulum stress pathways (Sedky and Magdy, 2021)