Comparison of plasma MicroRNA levels in drug naive, first episode depressed patients and healthy controls.

Major depression is the most common psychiatric disorder. The diagnosis of depression depends on a patient's subjective complaints, and the nature of the heterogeneous disorder. Thus, there is no known biomarker for depression to date. Previous research has indicated that microRNAs are dysregulated in bipolar disorder and schizophrenia. We aimed to investigate microRNA dysregulation in plasma samples of patients with major depression. Venous blood samples of 50 depressed patients and 41 healthy controls were collected and the quantification of microRNAs was established using qRT-PCR. We found miR-320a significantly downregulated and miR-451a significantly upregulated in depressed patients. We also found miR-17-5p and miR-223-3p upregulated, but not as significantly as miR-451a. Merging our results with previous published data shows that the blood miR-320 family may be a potential microRNA family dysregulated in major depression. Research should be performed on miR-320-related pathways and their relationship to depression. Additionally, miR-451a could serve as a candidate biomarker for depression based on the acting mechanism of ketamine. Studies targeting miR-451a levels before and after treatment could be helpful.

Effects of venlafaxine and fluoxetine on lymphocyte subsets in patients with major depressive disorder: a flow cytometric analysis.

BACKGROUND: Studies have yielded conflicting results concerning flow cytometric lymphocyte analyses in patients with depression. Data about the effect of antidepressants on lymphocyte subsets are also contradictory. The aim of this study was to determine effects of venlafaxine versus fluoxetine on lymphocyte subsets in depressive patients. METHODS: Sixty-nine patients diagnosed with major depressive disorder (MDD) according to DSM-IV and 36 healthy controls are included in the study. Sixty-nine patients were randomized to take fluoxetine (FLX) (n=33) or venlafaxine (VEN) (n=36). Serum lymphocyte subsets included CD3, CD4, CD8, CD16/56, CD19, CD45, Anti-HLA-DR which were measured by flow cytometric analyses at baseline and 6 weeks after the start of treatment. The severity of depression was evaluated with Hamilton rating scale for depression. RESULTS: At baseline, patients with MDD had significantly lower CD16/56 ratio and higher CD45 ratio compared to the controls. Although numerically higher in the VEN treated patients, treatment response rates between the FLX (53%) and the VEN (75%) groups were not different statistically. CD45 values decreased significantly in the VEN group at the end of the 6 week treatment period whereas no difference was observed in the FLX group. By the 6th week, treatment responders showed a significantly higher CD16/56 ratio than non-responders. Baseline severity of depression and anxiety was positively correlated with baseline CD45 ratio and negatively correlated with baseline CD16/56 ratio. We did not observe consistent changes in the absolute number of circulating B or T cells, nor in the helper/inducer (CD4) or suppressor/cytotoxic (CD8) subsets. CONCLUSIONS: CD16/56 was lower in patients with MDD and increased in treatment responders at 6th week. CD45 ratio was higher in patients with MDD than healthy subjects; it decreased with antidepressant treatment and was positively correlated with the severity of depression. Antidepressant treatment contributes to immune regulation in patients with major depressive disorder.

Effects of fluoxetine and venlafaxine on serum brain derived neurotrophic factor levels in depressed patients.

BACKGROUND: Several studies demonstrated that depressed patients had low serum BDNF levels which correlated with the severity of their depression, and antidepressant treatment increases levels of serum BDNF in depressed patients. It was speculated that agents acting on both noradrenergic and serotonergic transporters might have a greater influence on BDNF levels. The aim of our study was to determine effects of venlafaxine vs. fluoxetine on serum BDNF levels in depressive patients. METHODS: Forty-three patients diagnosed as major depressive disorder according to DSM-IV are included in the study. Forty-three patients were randomized to take fluoxetine (22 cases) or venlafaxine (21 cases). Serum levels of BDNF were measured by ELISA at baseline and 6 weeks after the start of treatment. RESULTS: Baseline levels of BDNF were not significantly different between the patient group and the controls. But male patients and the male controls showed statistical differences with respect to baseline BDNF levels. BDNF levels of the patient group did not change with treatment. Yet, the increase of BDNF levels was close to statistically significant in the fluoxetine group, whereas not significant in the venlafaxine group. There were no significant differences in baseline and 6th week BDNF levels between the responders and the non-responders. CONCLUSION: Further studies controlling for a wide variety of confounding variables are needed, which may help to reach a clear conclusion about the potential of BDNF as a biomarker for depression or as a predictor of antidepressant efficacy.

[Alopecia areata and alexithymia]. / Alopesi Areata ve Aleksitimi.

OBJECTIVE: Whether or not psychological factors play an important role in the pathogenesis of alopecia areata (AA) is a controversial issue. AA has had a tendency to be associated with high avoidance in attachment relationships, high alexithymic characteristics, and poor social support. Some studies have suggested that personality characteristics might modulate individual susceptibility to AA. The role of stressful life events in the appearance of AA is uncertain. In addition to reports associating anxiety and affective disorders with the onset of AA, there have also been studies that have not confirmed such an association. This case-control study was undertaken with the aim of determining the significance of stressful life events and other psychological factors in the etiopathogenesis of AA. METHOD: A total of 43 patients (26 male, 17 female) with AA and 53 age-and gender-matched healthy controls selected from hospital staff and their relatives (28 male, 25 female) were enrolled in the study. Both patients and controls were evaluated using the Hospital Anxiety and Depression Scale (HADS), Stress Scale, and Toronto Alexithymia Scale (TAS). RESULTS: There was no statistically significant difference between the patient and control groups with regard to the total scores of stressful major life events, depression, and anxiety (p>0.05). However, TAS scores in patients with AA were higher than in controls (p=0.013). CONCLUSION: The present study found no evidence that stressful major life events, depression, or anxiety have a role in the etiopathogenesis of AA, but AA tended to be associated with alexithymia. It has been suggested that alexithymics may suffer from unnoticed chronic stress with physiological, endocrine, and immune consequences, and that alexithymia is associated with impaired immune response. We suggest that alexithymia may play a role in the pathogenesis of AA via stress-induced immunological mechanisms.