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Optimizing brain functional-structural architecture with cTBS to reduce relapse in alcohol use disorder: a randomized
Zhou-Kang Wu1,2, Jing-Nan Zhao3, Ning-Ning Zeng4
1Department of Metabolic & Bariatric Surgery, Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, Shanghai, China.
Continuous theta-burst stimulation (cTBS) targeting the right dorsolateral prefrontal cortex (rDLPFC) reduced alcohol use disorder relapse risk. This neuromodulation approach improved brain network regulation and was linked to neuroplasticity, offering a promising intervention for AUD patients.
Area of Science:
- Neuroscience
- Psychiatry
- Medical Imaging
Background:
- Alcohol use disorder (AUD) is marked by high relapse rates, indicating a need for effective interventions.
- Continuous theta-burst stimulation (cTBS) over the right dorsolateral prefrontal cortex (rDLPFC) is a potential treatment for AUD by modulating brain networks involved in craving and self-control.
- The efficacy and underlying mechanisms of rDLPFC-targeted cTBS for AUD require further investigation.
Purpose of the Study:
- To evaluate the efficacy of rDLPFC-targeted cTBS in reducing relapse rates in AUD patients.
- To elucidate the neural mechanisms, including network control dynamics and gene expression, associated with cTBS treatment for AUD.
- To explore the evolutionary conservation of identified network-control targets.
Main Methods:
- A randomized, double-blind, sham-controlled trial involving 50 AUD patients.
- Patients received either active cTBS or sham stimulation over the rDLPFC for two weeks.
- Assessments included Alcohol Use Disorders Identification Test (AUDIT) scores, 1-year relapse monitoring, resting-state fMRI analyzed with NMF and TabPFN, network control theory (NCT), transcriptomic analysis, and cross-species phenotype mapping.
Main Results:
- Active cTBS significantly reduced the risk of relapse over one year compared to sham treatment (HR=0.426, p=0.041).
- cTBS enhanced an abstinence-associated neural pattern in prefrontal-subcortical regions (p=0.042) and reduced frontoparietal network (FPN) to subcortical network (SUB) control energy (p=0.003).
- Reduced control energy mediated improvements in alcohol-use severity (p<0.05) and correlated with neuroplasticity-related gene expression.
Conclusions:
- rDLPFC-targeted cTBS is associated with a lower risk of relapse in AUD patients.
- The therapeutic effect is potentially mediated by modulation of FPN-to-SUB network regulation, linked to neuroplasticity.
- Findings support network-informed neuromodulation as a viable strategy for AUD treatment, with conserved evolutionary targets.
