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Year : 2014  |  Volume : 39  |  Issue : 3  |  Page : 149-155

Analysis of human platelets brain-derived neurotrophic factor as a predictor of response in depressed patients

1 Department of Neuropsychiatry, Faculty of Medicine, Tanta University, Tanta, Egypt
2 Department of Clinical Pathology, Faculty of Medicine, Mansoura University, Mansoura, Egypt
3 Department of Internal Medicine, Faculty of Medicine, Mansoura University, Mansoura, Egypt
4 Department of Emergency Hospitals, Faculty of Medicine, Mansoura University, Mansoura, Egypt

Correspondence Address:
Abdulrahman Fahmi Alshaik
Department of Emergency Hospitals, Faculty of Medicine, Mansoura University, Algomhouria Street, Mansoura 35516
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1110-1067.148248

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Background Despite the significant progress in the management of major depressive disorder, little is known about the biological alterations that underlie the pathophysiology or the treatment of depression. Previous studies show that the brain-derived neurotrophic factor (BDNF) may play a role in the pathophysiology of major depressive disorders. Assuming that BDNF may be implicated in the etiology of depression, we examined BDNF concentrations in patients with major depressive disorder and its correlation with therapeutic response to fluoxetine therapy. Patients and methods This study included 40 depressed patients (25 women and 15 men) and 20 healthy individuals (11 women and nine men) as a control group selected to match the study group in age and sex. All patients were subjected a semistructured clinical interview of DSM-IV-TR for the diagnosis of major depressive disorder, assessment of severity of depression using the 16-item Hamilton Rating Scale of Depression before treatment and 8 weeks after fluoxetine treatment, and estimation of the level of BDNF before treatment and 8 weeks after antidepressant treatment. Results Before treatment, the concentrations of BDNF were significantly lower in depressed patients than in the control participants. After treatment, a significant increase in the BDNF concentration occurred, with no significant difference from the control group. Serum BDNF levels in patients with poor response (17.58 ± 4.99 ng/ml) were significantly lower than those of the patients with good response (28.88 ± 7.81 ng/ml; t = 5.48, P = 0.001). However, there were no significant differences in both groups of patients compared with the normal controls (21.60 ± 8.04). Conclusion BDNFs drug-free depressed patients are lower than those of healthy controls and we propose that low BDNF levels might reflect failure of neuronal plasticity in depression. Also, The increase in BDNF after antidepressant therapy could be considered a good predictor of response to antidepressant therapy and might contribute toward the therapeutic response of patients with major depressive disorder.

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