Serum brain-derived neurotrophic factor levels were reduced during methamphetamine early withdrawal
Related Experiment Video
Updated: May 23, 2026

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
Published on: January 22, 2016
Pao-Huan Chen1, Ming-Chi Huang, Ying-Ching Lai
1Department of Psychiatry and Psychiatric Research Center, Taipei Medical University Hospital, Taiwan, Department of Addiction Science, Taipei City Psychiatric Center, Taipei City Hospital, Taiwan, Department of Psychiatry, School of Medicine, Taipei Medical University, Taiwan, Department of Psychiatry, Cathay General Hospital, Taiwan Department of General Psychiatry, Taipei City Psychiatric Center, Taipei City Hospital, Taiwan.
Abstract:
Methamphetamine (METH) abuse is an increasing public health problem worldwide. Many of the METH-induced physical and mental problems are associated with the neurotoxic effects of METH. Animal studies have shown that brain-derived neurotrophic factor (BDNF) decreased after repeated amphetamine administration and increased at 30 and 90 days from psychostimulant withdrawal, suggesting that there might be a psychostimulant-induced neuroprotective dysfunction followed by a neuroadaptive process in the brain. However, current research on the role of BDNF in human METH addiction is limited, particularly during early withdrawal. The aim of this study was to assess the serum BDNF levels in METH abusers during the early withdrawal stage. Two groups of subjects were enrolled: (1) 59 DSM-IV METH abusers confirmed by board-certified psychiatrists during the first 3 weeks of withdrawal; (2) 59 age- and sex-matched healthy controls. We found that serum BDNF levels were significantly and constantly lower in the METH abusers during early withdrawal than those of the healthy controls. This indicates that METH abusers might have severe BDNF dysfunction and an impaired neuroprotective function after repetitive METH misuse.
Insights
Methamphetamine (METH) abuse is linked to lower brain-derived neurotrophic factor (BDNF) levels in early withdrawal. This suggests impaired neuroprotection in METH abusers, highlighting a potential target for addiction treatment.
Area of Science:
- Neuroscience
- Psychiatry
- Addiction Medicine
Background:
- Methamphetamine (METH) abuse presents a growing global health challenge, with neurotoxic effects contributing to physical and mental health issues.
- Animal studies indicate altered brain-derived neurotrophic factor (BDNF) levels during amphetamine withdrawal, suggesting neuroprotective dysfunction and subsequent adaptation.
- Limited research exists on BDNF's role in human METH addiction, especially during early withdrawal stages.
Purpose of the Study:
- To investigate serum BDNF levels in individuals undergoing early METH withdrawal.
- To compare BDNF levels between METH abusers in early withdrawal and healthy controls.
Main Methods:
- Enrolled 59 individuals diagnosed with DSM-IV METH abuse within the first three weeks of withdrawal.
- Recruited 59 age- and sex-matched healthy controls for comparison.
- Measured and compared serum BDNF levels between the METH abuser and control groups.
Main Results:
- Serum BDNF levels were significantly lower in METH abusers during early withdrawal compared to healthy controls.
- This reduction in BDNF was consistent throughout the early withdrawal period observed.
- The findings suggest a persistent dysfunction in BDNF levels among METH abusers.
Conclusions:
- METH abusers exhibit significantly lower serum BDNF levels during early withdrawal.
- This indicates a potential severe dysfunction in BDNF and impaired neuroprotective mechanisms following repeated METH misuse.
- The study underscores the importance of BDNF in the neurobiology of METH addiction and withdrawal.
More Related Videos
08:36Neurotoxicity Assessment in Adult Danio rerio using a Battery of Behavioral Tests in a Single Tank
Published on: November 3, 2023
11:44Cellular Membrane Affinity Chromatography Columns to Identify Specialized Plant Metabolites Interacting with Immobilized Tropomyosin Kinase Receptor B
Published on: January 19, 2022