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Possible mechanisms make clinical sense The simulated mechanisms outlined in this new research are plausible: GLP-1 receptor agonism may up-regulate synaptic recovery or alter SNAP-25 phosphorylation, thereby shortening the effective blockade period of BoNT-A Lean-mass decline is common in GLP-1 induced weight loss and could alter diffusion or the volume of distribution of injected toxin, reducing dwell-time in muscle tissue Metabolic alterations, such as changes in clearance and/or muscle repair dynamics, may accelerate neuromuscular recovery

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