Brain-Derived Neurotrophic Factor Serum Levels in Alcohol-Dependent Subjects 6 Months After Alcohol Withdrawal
Article first published online: 16 AUG 2011
Copyright © 2011 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 35, Issue 11, pages 1966–1973, November 2011
How to Cite
Costa, M.-A., Girard, M., Dalmay, F. and Malauzat, D. (2011), Brain-Derived Neurotrophic Factor Serum Levels in Alcohol-Dependent Subjects 6 Months After Alcohol Withdrawal. Alcoholism: Clinical and Experimental Research, 35: 1966–1973. doi: 10.1111/j.1530-0277.2011.01548.x
- Issue published online: 1 NOV 2011
- Article first published online: 16 AUG 2011
- Received for publication September 17, 2010; accepted March 9, 2011.
- Alcohol Dependence;
- Neuronal Plasticity
Background: Diagnosing alcohol dependence is based on clinical signs and on the measured levels of biological markers of alcohol consumption. However, these markers are neither sufficiently sensitive and nor specific enough to definitively determine alcohol dependence. The neuroadaptive changes associated with alcohol dependence involve markers such as brain-derived neurotrophic factor (BDNF), which regulate neuronal plasticity. Serum levels of BDNF have been reported to decrease during alcohol dependence and may be restored to normal soon after alcohol is withdrawn. However, the long-term relationship between serum BDNF levels and abstinence status is unknown.
Methods: We investigated serum BDNF levels in 101 abstinent and relapsing alcohol-dependent subjects at the moment of hospitalization for alcohol withdrawal (M0) and 6 months later (M6) and compared them to the serum BDNF levels of 41 nondependent subjects. The BDNF levels of the alcohol-dependent subjects were compared to their serum gamma glutamyl transferase (GGT) levels, mean corpuscular volume (MCV) values, and their score on the Beck Depression Inventory (BDI) questionnaire.
Results: Forty-four percent of the alcohol-dependent participants remained abstinent during the 6 months following alcohol detoxification. Serum BDNF levels of the abstinent group at M6 were significantly higher than those of the original group of alcohol-dependent subjects at M0 (p = 0.034). Only the abstinent group had higher BDNF levels than the control group (p < 0.001). Serum BDNF levels increased to a greater extent in the abstinent group than in the nonabstinent group (p = 0.016). No correlations were found between serum BDNF levels and GGT level, MCV value, or BDI score.
Conclusions: Our data confirm that serum BDNF levels do not correlate with either chronic alcohol consumption or peripheral toxicity but may be linked to neuronal aspects of alcohol consumption and dependence. The increased serum levels of BDNF may reflect the concomitant activation of BDNF synthesis that accompanies the neuronal remodeling triggered by alcohol withdrawal and suggests that BDNF synthesis may have a role in the long-term maintenance of abstinence. Monitoring the serum BDNF levels of alcoholics undergoing treatment could help to characterize alcohol dependence profiles and predict relapse.