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Early data show benefits of glucagon-like peptide-1 receptor agonists in halting the progression of this progressive neurologic disorder, which stems from a dopamine deficiency

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In islet alpha cells, GLP-1(936) led to inhibition of Ca2+ entry via voltage-gated Ca2+ channels sensitive to -agatoxin, with consequential pertussis-toxin-sensitive depletion of the docked pool of secretory granules, effects that were prevented by the glucagon receptor antagonists REMD2.59 and L-168049