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Related Concept Videos

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CNS Depressants: Alcohol and Nicotine

Ethanol, a clear colorless alcohol, has been consumed by humans for millennia, but its effects on the body are far from benign. At lower doses, it induces decreased inhibitions and loquaciousness, leading to its social appeal. However, it can cause severe consequences at higher doses, such as coma and respiratory depression, due to its zero-order elimination kinetics. Chronic ethanol abuse wreaks havoc on multiple organ systems, particularly the CNS and the liver. Abrupt cessation of ethanol...
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Related Experiment Video

Updated: May 18, 2026

Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder
05:12

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Published on: June 23, 2023

Continuous Theta-Burst Stimulation Improves Long-Term Outcomes in Alcohol Use Disorder by Modulating a

Liang-Jie-Cheng Huang1, Ning-Ning Zeng2, Jing-Nan Zhao3

  • 1Department of Psychology, Ningbo University, Ningbo, China.

Biological Psychiatry
|May 16, 2026
PubMed
Summary
This summary is machine-generated.

Continuous theta-burst stimulation (cTBS) significantly reduced drinking in alcohol use disorder (AUD) patients over 12 months. This circuit-based therapy shows promise for addiction by modulating neural networks involved in craving.

Keywords:
Alcohol use disorderContinuous theta-burst stimulationCravingDrinking reductionFunctional connectivityLong-term efficacy

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Area of Science:

  • Neuroscience
  • Addiction Medicine
  • Psychiatry

Background:

  • Alcohol use disorder (AUD) is a chronic relapsing condition marked by craving.
  • Continuous theta-burst stimulation (cTBS) is a potential treatment for AUD, but its long-term effects and mechanisms require further investigation.

Purpose of the Study:

  • To evaluate the 12-month efficacy of right dorsolateral prefrontal cortex (DLPFC) cTBS for reducing alcohol consumption.
  • To identify neural and molecular mechanisms underlying cTBS treatment for AUD.

Main Methods:

  • Fifty-five alcohol-dependent patients received 20 sessions of active or sham cTBS over two weeks.
  • Clinical outcomes were assessed over 12 months, including drinking behavior and craving.
  • Functional MRI during a cue-reactivity task was used to investigate craving-related neuroplasticity.

Main Results:

  • Active cTBS significantly reduced the risk of returning to baseline or higher drinking levels compared to sham treatment over 12 months.
  • Significant improvements were observed in Alcohol Use Disorders Identification Test (AUDIT) scores and subjective craving.
  • Changes in a craving-related neural network, involving frontoparietal, subcortical, visual, and ventral attention systems, correlated with clinical improvements.

Conclusions:

  • cTBS demonstrates long-term clinical efficacy in reducing alcohol consumption for individuals with AUD.
  • The study identified a multiscale biomarker linked to synaptic transmission and myelination, offering insights into cTBS's therapeutic mechanisms.
  • cTBS presents a promising circuit-based therapy for addiction treatment.