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Activation of nicotinic acetylcholine receptors can suppress the downstream mechanisms of excitotoxicity, including intracellular Ca 2+ overload, increased ROS, and mitochondrial energy metabolism disorders

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The primary endpoint was to identify changes in plasma metabolic profiles following the GF-MKD intervention

This increase in DAT function stems at least in part from augmented DAT surface expression, pointing to DAT trafficking as the underlying mechanism by which GLP-1R signaling and AA levels controls DA homeostasis in the LS, as depicted by our schematic model (Supplementary Figure 5)