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Brain Sciences
Special Issues
Risks and Mechanisms in Addiction Neuroscience Informing Treatment
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Risks and Mechanisms in Addiction Neuroscience Informing Treatment

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuropsychiatry".

Deadline for manuscript submissions: 15 October 2026 | Viewed by 2608

Editor

Dr. Amy A. Herrold

E-Mail Website
Guest Editor
Department of Psychiatry and Behavioral Sciences, Northwestern University, Chicago, IL 60654, USA
Interests: addiction; traumatic brain injury; psychiatry

Special Issue Information

Dear Colleagues,

Tremendous advances have been made in our understanding of addiction cycle neurocircuitry. These advances have propelled further research into mechanisms and risk in addiction neuroscience, informing novel treatment development; this Special Issue aims to highlight this research.

We are looking for cutting-edge research on novel risks and mechanisms which may inform treatment, such as co-occurring conditions that confer addiction risk (e.g., traumatic brain injury), neuromodulatory treatments (e.g., transcranial magnetic stimulation), novel therapeutic plastogens (e.g., psychedelics), exercise treatment interventions (e.g., yoga) and endocrine system approaches (e.g., GLP-1 receptor agonists)

We welcome original research reports, scoping reviews, systematic reviews and meta-analyses.

Dr. Amy A. Herrold
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • substance use disorders
  • risk
  • mechanism
  • neuromodulation
  • psychedelic
  • GLP-1

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Published Papers (3 papers)

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Research

Jump to: Review

12 pages, 812 KB  
Article
Fentanyl Induces Behavioral Sensitization and Decreases Class IIa HDAC Expression-Activity in Brain as Measured by [18F]TFAHA PET Imaging in Female and Male Rats
by Cameron J. Davidson, Itzick Nahmoud, Mahmoud Teran, Erek Binkowski, Nareen Sadik, Majd A. Yahya, Susanne Brummelte, Alana C. Conti, Nerissa T. Viola, Srinivasu Kallakuri and Shane A. Perrine
Brain Sci. 2026, 16(7), 684; https://doi.org/10.3390/brainsci16070684 - 29 Jun 2026
Viewed by 248
Abstract
Background: Although fentanyl significantly contributes to opioid-related morbidity and mortality, little is known about the epigenetic changes that may influence long-term neuronal adaptations. Objective: The effects of repeated fentanyl administration on class IIa histone deacetylase (HDAC) expression-activity were studied using the radiotracer [ [...] Read more.
Background: Although fentanyl significantly contributes to opioid-related morbidity and mortality, little is known about the epigenetic changes that may influence long-term neuronal adaptations. Objective: The effects of repeated fentanyl administration on class IIa histone deacetylase (HDAC) expression-activity were studied using the radiotracer [18F]TFAHA and positron emission tomography (PET) imaging in a model of fentanyl-induced behavioral sensitization. Methods: Female and male Wistar rats received 14 days of fentanyl (20 μg/kg) or saline injections and a 14-day drug-free period followed by a single fentanyl or saline challenge dose on day 28. Locomotor activity (LMA) was measured on days 0, 1, 14, and 28 with PET imaging being performed at baseline and again on day 28 following the fentanyl/saline challenge and LMA. The percent change in standard uptake value (body weight corrected) between pre- and post-administration was calculated as a measure of class IIa HDAC expression-activity. Results: Repeated fentanyl exposure resulted in significantly increased LMA in both sexes compared to controls. Females displayed an earlier onset (day 1) and a greater magnitude of behavioral sensitization on days 14 and 28 compared to males. Fentanyl significantly decreased class IIa HDAC expression-activity across time in the whole brain and in reward-related brain regions without sex differences. Conclusions: Prolonged fentanyl exposure induces robust sex-specific locomotor sensitization with varying magnitude over time, suggesting differential neuroadaptive processes. Fentanyl also appears to induce epigenetic changes in the brain independent of sex and region. The effect of fentanyl on class II HDACs may not directly impact the expression of behavioral sensitization. Full article
(This article belongs to the Special Issue Risks and Mechanisms in Addiction Neuroscience Informing Treatment)
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17 pages, 1175 KB  
Article
Effects of a Single Sub-Anesthetic Dose of Ketamine in Tobacco Use Disorder: An Active-Placebo, Randomized Crossover Study
by Nathan R. Luzum, Marcia H. McCall, Charlotte Talley Boyd, Heather Columbano, Edward Ip, Santiago Saldana, Alison H. Oliveto and Merideth Addicott
Brain Sci. 2026, 16(5), 496; https://doi.org/10.3390/brainsci16050496 - 30 Apr 2026
Viewed by 773
Abstract
Background/Objectives: A sub-anesthetic dose of ketamine has shown promise in reducing craving, withdrawal symptoms, and use of drugs such as alcohol, cocaine, and opioids among individuals with substance use disorders. Ketamine’s therapeutic potential for tobacco use is unknown. Here, we investigated a single [...] Read more.
Background/Objectives: A sub-anesthetic dose of ketamine has shown promise in reducing craving, withdrawal symptoms, and use of drugs such as alcohol, cocaine, and opioids among individuals with substance use disorders. Ketamine’s therapeutic potential for tobacco use is unknown. Here, we investigated a single sub-anesthetic dose among adults with tobacco use disorder who were not interested in changing their smoking behavior. Methods: Utilizing a randomized, within-subject crossover, double-blinded, counter-balanced, midazolam-controlled design, participants (n = 18) received a 0.71 mg/kg infusion of ketamine and a 0.025 mg/kg infusion of midazolam (i.e., active placebo) at least two weeks apart. Participants were asked to abstain from smoking after the infusions until the post-infusion sessions, 1 day following infusion, where participants completed measures of smoking behavior, craving, and withdrawal symptoms. Participants continued to record their smoking behavior over the 7 days following infusion. Participants also completed a semi-structured qualitative interview regarding their experiences. Results: Compared to midazolam, ketamine infusion led to a non-significant reduction (p = 0.10, ηp2 = 0.153) in the number of cigarettes smoked during the requested abstinence period. Following this period, there were no significant differences in ad lib smoking. Ketamine showed no effect on craving or withdrawal symptoms. Participants reported more intense psychological experiences following ketamine infusion (p < 0.001, ηp2 = 0.830) and about half reported it felt easier to abstain from smoking after the ketamine infusion. Conclusions: While well tolerated, these findings suggest ketamine has little to no direct effect on quantitative measures of cigarette smoking, craving, or withdrawal. However, the qualitative measures suggest ketamine improves mood and reduces craving in some individuals for several days. Future studies should investigate whether ketamine can indirectly support smoking cessation among individuals with comorbid psychiatric indications for ketamine treatment. Full article
(This article belongs to the Special Issue Risks and Mechanisms in Addiction Neuroscience Informing Treatment)
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Review

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17 pages, 994 KB  
Review
MAC/MAB–RCS: An Integrative Regulatory Control Framework for Risk Stratification and Personalized Intervention in Addiction Psychiatry
by Anna Makarewicz, Remigiusz Recław, Anna Grzywacz, Jolanta Chmielowiec and Krzysztof Chmielowiec
Brain Sci. 2026, 16(2), 187; https://doi.org/10.3390/brainsci16020187 - 3 Feb 2026
Viewed by 823
Abstract
Objectives: Addiction disorders remain a major challenge in contemporary psychiatry due to high relapse rates and significant individual and societal burden. Despite advances in addiction neurobiology, current diagnostic frameworks and dominant models offer limited tools for early risk identification and dynamic support of [...] Read more.
Objectives: Addiction disorders remain a major challenge in contemporary psychiatry due to high relapse rates and significant individual and societal burden. Despite advances in addiction neurobiology, current diagnostic frameworks and dominant models offer limited tools for early risk identification and dynamic support of clinical decision-making across the course of treatment. The aim of this narrative review is to introduce the MAC/MAB–RCS model as an integrated conceptual framework for risk stratification and personalized intervention in addiction psychiatry. Methods: The proposed model integrates evidence from four complementary domains: genetic, epigenetic, and stress-axis biomarkers; functional brain network organization; and psychological/psychiatric dimensions relevant to addictive behaviors. These domains are synthesized into a unified conceptual structure designed to capture dynamic regulatory processes underlying addiction vulnerability. Results: At the core of the model lies the Regulatory Control State (RCS), a latent higher-order construct representing an individual’s dynamic regulatory capacity through the integration of cognitive control, emotional regulation, and motivational drive modulation. Disruption of the RCS is conceptualized as a shared transdiagnostic mechanism driving craving escalation, compulsive behavior, and relapse vulnerability, independent of substance class or specific addictive behavior. Conclusions: The MAC/MAB–RCS model aligns with the principles of precision psychiatry by offering a pragmatic, clinically oriented translational framework with potential applicability across clinical settings, bridging neurobiological research and clinical practice. The review discusses its relationship to existing models, potential clinical and systemic applications, key limitations, and priorities for future validation studies. Full article
(This article belongs to the Special Issue Risks and Mechanisms in Addiction Neuroscience Informing Treatment)
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