Alterations in Serum BDNF Levels in Early Alcohol Withdrawal and Comparison with Healthy Controls


Cavus S. Y., Dilbaz N., Darcin A. E., EREN F., Kaya H., Kaya O.

KLINIK PSIKOFARMAKOLOJI BULTENI-BULLETIN OF CLINICAL PSYCHOPHARMACOLOGY, cilt.22, sa.3, ss.210-215, 2012 (SCI-Expanded) identifier identifier

Özet

Alterations in serum BDNF levels in early alcohol withdrawal and comparison with healthy controls Objective: A protective effect of BDNF against ethanol induced cell damage has been suggested, and this effect may contribute to the development of alcohol dependence. Although the mechanisms involved in chronic alcohol treatment-induced neurotoxic actions have not yet been clearly identified, recent studies have hypothesized that prolonged alcohol intake may affect the synthesis of neurotrophins, which are a family of proteins that play a crucial role in cognitive functions, including learning and memory. One of these neurotrophins, BDNF, has a significant role in neuronal development, plasticity, and learning, There are also various study results showing a modulatory role of BONE in the development and maintenance of addictive behaviour. In this study, we aimed to determine the changes of serum BONE levels in alcoholic patients at the first and seventh days of withdrawal and compare that to those of healthy controls in order to determine the role of BDNF in alcohol dependence. Method: A total of 31 male patients suffering from alcohol dependence according to the DSM-IV-TR were admitted for alcohol detoxification treatment and 29 healthy control subjects were enrolled in the study. Patients suffering from psychiatric diagnoses apart from alcohol and nicotine dependence were excluded from the study. Further exclusion criteria were substance abuse other than alcohol or nicotine, severe neurological diseases like cerebral ischemia or haemorrhage, epilepsy, cardiovascular and renal diseases, former delirium tremens, and use of psychopharmacological medication. Alcoholic patients were treated with diazepam in order to prevent alcohol withdrawal symptoms. The dose of diazepam was tapered gradually by monitoring alcohol withdrawal severity (minimum: 30 mg, maximum: 40 mg on day 1) during alcohol withdrawal. The severity of withdrawal symptoms was evaluated by the Clinical Institute Withdrawal Assessment-Alcohol, Revised (CIWA-AR) every eight hours. Blood samples of the patient group were collected on the first and seventh day of alcohol withdrawal, and centrifuged and stored at -70 degrees C immediately after collection. Serum BDNF levels were measured using a sandwich enzyme-linked immunosorbent assay (ELISA). The study was approved by the local ethics committee and all participants gave written informed consent prior to enrollment in the study. Results: Serum BDNF levels were significantly lower in the alcoholic patients compared with control subjects. (52.9 +/- 19.0 ng/ml and 65.3 +/- 15.9ng/ml, respectively, p=0.018) Furthermore, BDNF levels were found to be significantly decreased on the seventh day of withdrawal compared to that at baseline. (from 52.9 19.0 ng/ml to 33.5 +/- 8.8 ng/ml, p <= 0.001). The BDNF levels did not significantly correlate with clinical characteristics such usage, amount of alcohol consumption in the last month, duration of intake, or family history. Conclusion: This study suggests chronic drinking leads to a reduction in BDNF levels compared to those of healthy controls, implying that BDNF may have a role in the development of alcohol dependence and there is no elevation to that of control BDNF levels in the early alcohol withdrawal period. Further research will be necessary in order to identify the pathophysiological mechanisms and causalities that regulate BDNF plasma levels following alcohol intoxication and withdrawal. These studies should consider both early and late withdrawal periods and should be conducted in large samples in order to identify the association between the disorder and peripheral BDNF levels.