Journal article
A. Ceceli, S. King, K. Drury, N. McClain, John H. Gray, P. S. Dassanayake, J. Newcorn, Daniela Schiller, N. Alia-Klein, Rita Z. Goldstein
medRxiv, 2025
medRxiv, 2025
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DOI
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APA
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Ceceli, A., King, S., Drury, K., McClain, N., Gray, J. H., Dassanayake, P. S., … Goldstein, R. Z. (2025). The neural signature of methylphenidate-enhanced memory disruption in human drug addiction: a randomized clinical trial. MedRxiv.
Chicago/Turabian
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Ceceli, A., S. King, K. Drury, N. McClain, John H. Gray, P. S. Dassanayake, J. Newcorn, Daniela Schiller, N. Alia-Klein, and Rita Z. Goldstein. “The Neural Signature of Methylphenidate-Enhanced Memory Disruption in Human Drug Addiction: a Randomized Clinical Trial.” medRxiv (2025).
MLA
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Ceceli, A., et al. “The Neural Signature of Methylphenidate-Enhanced Memory Disruption in Human Drug Addiction: a Randomized Clinical Trial.” MedRxiv, 2025.
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@article{a2025a,
title = {The neural signature of methylphenidate-enhanced memory disruption in human drug addiction: a randomized clinical trial},
year = {2025},
journal = {medRxiv},
author = {Ceceli, A. and King, S. and Drury, K. and McClain, N. and Gray, John H. and Dassanayake, P. S. and Newcorn, J. and Schiller, Daniela and Alia-Klein, N. and Goldstein, Rita Z.}
}
Abstract
Background: Drug-related memories can hinder abstinence goals in drug addiction. Promoting non-drug memories via ventromedial prefrontal cortex- (vmPFC) and amygdala-guided extinction yields mixed success. Post-retrieval extinction (RE) destabilizes and updates memories during reconsolidation, improving extinction. Supplementing RE, we tested methylphenidate (MPH), a dopamine-agonist that promotes PFC-dependent learning and memory in cocaine use disorder (CUD). In an Early Phase 1 double-blind randomized clinical trial using a within-subjects design, participants received oral MPH (20 mg) or placebo before the retrieval of some of the conditioned stimuli (i.e., reminded CS+ vs. non-reminded CS+) followed by extinction; lab-simulated drug-seeking was measured the following day. Results: Lower vmPFC activity following non-reminded CS+ (standard extinction) under placebo replicated the putative impairments in CUD; separately, RE (trend) and MPH conditions recruited the vmPFC, and RE's vmPFC-reliance correlated with drug-seeking only under placebo. Crucially, MPH-combined RE normalized cortico-limbic processing, bypassing the vmPFC and its amygdala connectivity. Conclusions: Pharmacologically-enhanced drug memory modulation may inform intervention development for addiction recovery.