Researchers have reported that serum brain-derived neurotrophic factor (sBDNF) of drug-free depressed patients are lower than those of healthy controls and proposed that low sBDNF levels might reflect failure of neuronal plasticity in depression. In this study, we compared sBDNF levels of depressed patients (n = 28) before and after 8 weeks of antidepressant treatment, with those of healthy controls (n = 18) to test the hypothesis that initially low sBDNF levels of drug-free depressed patients will increase parallel with their clinical response to antidepressant treatment. The severity of depression and response to treatment were assessed with Hamilton Rating Scale for Depression (HAM-D). sBDNF was assayed with the sandwich ELISA method. Baseline sBDNF levels of patients (mean, 20.8 ng/ml; [S.D., 6.7]) were significantly lower than those of controls (mean, 26.8 ng/ml; [S.D., 9.3]; p = 0.015), and were negatively correlated with HAM-D scores (r = -0.49, p = 0.007). After 8 weeks of treatment, sBDNF levels of patients had increased significantly (mean, 33.3 ng/ml; [S.D., 9.9]; p < 0.001) and no longer differed from those of controls. These results support the hypothesis that BDNF might play a critical role in the pathophysiology of major depressive disorder and successful antidepressant treatment increases the attenuated BDNF levels in depressed patients.

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Although many studies have examined the neurobiological aspects of suicide, the molecular mechanisms and pathophysiologic mechanisms associated with suicide remain unclear. In this study, it is aimed to investigate whether there is a difference in serum brain-derived neurotrophic factor (BDNF) levels among suicide attempters without a major psychiatric disorder, compared to major depressive disorder patients and healthy subjects. It was undertaken with the hypothesis that suicide per se lowers serum BDNF levels, since it is a source of stress. The study was carried out in Celal Bayar University Hospital, Manisa, Turkey. Ten suicide attempters, 24 patients with major depressive disorder and 26 subjects without any psychiatric diagnosis and any psychiatric treatment were included in the study. All subjects were asked to give their written consent. Blood samples were collected at the baseline. Serum BDNF was kept at –70°C before testing, and assayed with an ELISA kit (Promega; Madison, Wisc., USA) after dilution with the block and sample solution provided with the kit. The data were subjected to the Kruskal-Wallis test for nonparametric analysis of variance. Mean serum BDNF levels were significantly lower in the suicide group (21.2 ± 12.4 ng/ml) and the major depressive disorder group (21.2 ± 11.3 ng/ml) than the control group (31.4 ± 8.8 ng/ml; p = 0.004). These results suggest that BDNF may play an important role in the neurobiology of suicidal behavior. BDNF levels may be a biological marker for suicidal behavior. To investigate the role of BDNF in suicide, further studies with a wider sample size and a variety of psychiatric diagnoses accompanying suicide attempt are needed.