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Dinko Franceschi

Researcher at Stony Brook University

Publications -  72
Citations -  6042

Dinko Franceschi is an academic researcher from Stony Brook University. The author has contributed to research in topics: Dopamine & Raclopride. The author has an hindex of 26, co-authored 67 publications receiving 5773 citations. Previous affiliations of Dinko Franceschi include Lund University & State University of New York System.

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Association of Dopamine Transporter Reduction With Psychomotor Impairment in Methamphetamine Abusers

TL;DR: Evidence is provided that methamphetamine at dose levels taken by human abusers of the drug leads to dopamine transporter reduction that is associated with motor and cognitive impairment and the urgency of alerting clinicians and the public of the long-term changes that methamphetamine can induce in the human brain.
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Low Level of Brain Dopamine D2 Receptors in Methamphetamine Abusers: Association With Metabolism in the Orbitofrontal Cortex

TL;DR: The association between level of dopamine D2 receptors and metabolism in the orbit ofrontal cortex in methamphetamine abusers suggests that D2 receptor-mediated dysregulation of the orbitofrontal cortex could underlie a common mechanism for loss of control and compulsive drug intake in drug-addicted subjects.
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Therapeutic doses of oral methylphenidate significantly increase extracellular dopamine in the human brain.

TL;DR: There is direct evidence that oral methylphenidate at doses within the therapeutic range significantly increases extracellular DA in human brain, and this result coupled with recent findings of increased dopamine transporters in ADHD patients provides a mechanistic framework for the therapeutic efficacy of methyl phenidate.
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Loss of Dopamine Transporters in Methamphetamine Abusers Recovers with Protracted Abstinence

TL;DR: It is suggested that protracted abstinence may reverse some of methamphetamine-induced alterations in brain DA terminals, and neuropsychological tests did not improve to the same extent as during short abstinence, which suggests that the increase of the DA transporters was not sufficient for complete function recovery.
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"Nonhedonic" food motivation in humans involves dopamine in the dorsal striatum and methylphenidate amplifies this effect.

TL;DR: The results provide the first evidence that dopamine in the dorsal striatum is involved in food motivation in humans that is distinct from its role in regulating reward through the NA, and the ability of methylphenidate to amplify weak dopamine signals is demonstrated.