ABSTRACT
Studies in recent years have indicated that neuroimmunological events and immune activation may have a place in the etiology of depression. It has been suggested from data that there is a causal relationship between activation of the immune system and excessive release of proinflammatory cytokines, such as interleukin 1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-alpha), and the etiology of depression. Although the mechanism of action of electroconvulsive therapy (ECT) is unclear, there is evidence that it can reduce cytokines and immune system changes. In our study, we aimed to determine how levels of serum immunomodulators were affected by ECT in major depression patients. This study was conducted on 50 patients with treatment-resistant major depression. The data of the patients were compared with 30 healthy individuals with similar demographic characteristics. A clinical response occurred in the patients and at the end of therapy, IL-1, IL-6, TNF-alpha, IL-10, IL-4, and interferon-gamma levels were measured. The disease severity was assessed with the 17-item Hamilton Depression Rating Scale. Data analysis was performed using SPSS Version 15. Significant differences were determined between the patients with major depression and control group with respect to basal serum IL-1, IL-6, TNF-alpha, IL-10, IL-4, and interferon-gamma levels. ECT treatment was shown to reduce these differences. ECT may cause significant changes in the activity of the immune system. The consideration of the relationship between the immune endocrine neurotransmitter systems could contribute to new theories regarding the mechanism of antidepressant treatment and biology of depression.
ABSTRACT
OBJECTIVES: This study aimed to investigate the effects of electroconvulsive treatment on serum BDNF and NGF levels in patients with treatment-resistant major depression. METHODS: Thirty patients with treatment-resistant major depression and 30 healthy controls were included in the study. The patients' serum BDNF and NGF levels were measured three times; before treatment (T0), when the clinical response occurred (T1) and at the end of treatment (T2). RESULTS: The reduction detected in the HAM-D scores with ECT during the T0-T1, T1-T2 and T0-T2 periods was found to be statistically significant. In the patient group, increase in the mean BDNF levels after ECT treatment was found to be statistically significant (p<0.05). Significant increases in serum BDNF levels with ECT were lower than in the control group, and the serum NGF levels did not increase significantly. There was no relationship between the severity of the depression and serum BDNF and NGF levels (p>0.05). CONCLUSIONS: This study evaluated the role of neurotrophic factors in the etiopathogenesis of major depression. Future studies should investigate the relationship between neurotrophic factors with neuroendocrine and genetic processes to elucidate the psychobiology and treatment of mental disorders.
