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When released (e.g., with vesicle depletion by reserpine or amphetamine) [69,70,152] it can substitute disturbed dopamine (i.e., shortage (reserpine) [69] or excess (amphetamine) [70]) as competing successfully for sites at dopamine receptors (i.e., counteracting the adverse effects of both dopamine agonists [70,152,153] and dopamine antagonists [68,70,152])

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More recently, alternative hypotheses to an amyloid-based mechanism for AD causality have been proposed

Appetite suppression is not the primary mechanism