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This review offers a comprehensive overview of how psychostimulants like cocaine and methamphetamine disrupt dopamine synthesis, storage, release, and reuptake, examines the neurobiological consequences of these disruptions, and proposes directions for future research on mechanisms and the development of novel neuroprotective therapies

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elegans expressing either human mutant α-synuclein (A53T) or human mutant LRRK2 (G2019S) exhibited deficits in this dopamine-related behavior (Cooper et al., 2015)