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Despite intense research efforts undertaken by investigators throughout the world over the past half century to identify a specific biomarker for major depressive disorder (MDD), none have so far met the rigorous test of specificity, reliability and reproducibility. Vascular Endothelial Growth Factor (VEGF) has been implicated in the neurotrophic model of depression and several studies have assessed VEGF levels in depressed patients. The results have been discrepant largely due to design and assay differences among studies. The aim of this study was to assess plasma VEGF levels in a cohort of MDD subjects prior to treatment with psychotropic medication and compare them to those of healthy control (HC) subjects. Prospective study participants underwent extensive medical and psychiatric assessments before they were enrolled. Plasma concentrations of VEGF were measured by the technique marketed by Randox Technologies. The mean baseline VEGF for the healthy and depressed groups was 5.91 pg/ml (SD: 3.04) and 10.51 pg/ml (SD: 9.04), respectively, and this difference was statistically significant (p = 0.001). We detected a very low univariate relationship between VEGF and demographic and clinical variables. Using the Optimal Data Analysis a cut score of 6.64 pg/ml for baseline plasma VEGF distinguished depressed from healthy subjects with a 63% overall accuracy. We conclude these results support a role of plasma VEGF as a useful biomarker of depression that can be measured with a routine blood draw at the point of service. The specificity of this potential biomarker must be confirmed in studies that include other psychiatric disease entities., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

TNF-α plays a key role in inflammatory responses, and its dysregulation has been implicated in a variety of human diseases. TNF-α has been shown to be elevated in depressed patients, suggesting a potential role as a biomarker in depression. In this analysis, we assessed the relationship between depression severity and TNF-α and determined whether monotherapy with either escitalopram, an SSRI, or the atypical antipsychotic, quetiapine, significantly affected serum TNF-α. In two consecutively run studies, after full psychiatric assessment, patients received either 12weeks of monotherapy with escitalopram or quetiapine. In addition to several other psychiatric and physiological parameters, TNF-α, HAMD, HAMA, and PSS-14 were measured at baseline and at weeks 8 and 12. Depressed patients demonstrated significantly higher TNF-α than healthy controls at baseline. Though TNF-α tended to decrease after treatment with escitalopram, neither treatment was shown to lead to significantly different TNF-α levels from those of baseline. No significant correlation could be demonstrated between treatment response and TNF-α at baseline in the escitalopram cohort or at any time in subjects receiving quetiapine. As expected, baseline TNF-α was elevated in depressed subjects and correlated positively with depression severity. Monotherapy with either escitalopram or quetiapine does not significantly alter TNF-α after 12weeks of treatment, and no correlation could be demonstrated between treatment response and TNF-α. [ABSTRACT FROM AUTHOR]

Interleukin-6 is a pro-inflammatory cytokine that stimulates the HPA-axis, sympathetic nervous system, and production of acute-phase reactants. Elevations of IL-6 have been reported in patients with major depressive disorder (MDD). Further studies have suggested that IL-6 is an indicator of the severity of symptoms, especially suicidality. Forty-eight MDD patients and 23 healthy subjects were analyzed from two consecutive studies of identical design. Subjects met DSM-IV criteria for primary MDD. Severity of depression was assessed using the HAMD-17 scale. Anxiety was assessed with the HAMA scale. Patients in the first study were treated for 12weeks with escitalopram. In the second study, patients received quetiapine XR for 12weeks with flexible dosing. The data for IL-6 were not normally distributed, so non-parametric tests were used for statistical analyses. Patients with MDD (n =48) had significantly higher baseline serum IL-6 than healthy controls (n =20) (p =0.05). Serum IL-6 failed to normalize with either escitalopram or quetiapine after treatment. Treatment response (⩽50% reduction or ⩽7 in HAM-D17 score) did not correlate with baseline level of IL-6. There was a significant correlation between baseline IL-6 and depression severity as measured by HAMD-7 (p =0.05). This significance was lost with the HAMD-17 scale. There were no correlations between baseline IL-6 and severity of anxiety. Age was the only confound as younger MDD patients (<39yrs) had higher IL-6 than healthy controls (p =0.01). [ABSTRACT FROM AUTHOR]