Dear colleagues,
It is my great pleasure to introduce to you the last issue of 2017 featuring original research on biomarkers and treatment response in depression.
Dietrich-Muszalska et al., review the platelet haemostatic function in psychiatric disorders as well as the effects of antidepressants and antipsychotic medication. Increased activation of platelets seen in patients with depression and schizophrenia is involved in cardiovascular diseases that may be a major cause of morbidity and mortality of patients. Use of antidepressants and antipsychotics in depression and schizophrenia is often associated with various haematological side effects. Improved understanding of platelet activation in depression and schizophrenia and medication may improve future therapeutics.
Clark-Raymond and associates investigated the baseline plasma vascular endothelial growth factor (VEGF) levels in major depressive patients as a possible predictor of antidepressant response. A difference in plasma VGEF levels was detected between remitters and non-responders. Their results suggest that VGEF may predict response to antidepressant treatment that may prove to be a potential biomarker, which can be measured during routine blood draw.
Jiang and colleagues evaluated whether serum VGF levels change in major depressive disorder (MDD) patients and if antidepressant treatment can restore those changes. They found VGF level to be significantly lower in MDD patients compared to controls and were reversed after 8 weeks of antidepressant treatment. VGF may be involved in the pathophysiology of MDD and in the underlying mechanisms of antidepressant action.
Wang et al., profiled the expression of mitochondrial genes in the dorsolateral prefrontal cortex (dlPFC) in MDD patients in comparison to healthy controls. They found 16 differentially expressed genes in MDD patients compared to controls. They conclude that abnormal mitochondrial systems in the brain of MDD subjects could be involved in the etiopathogenesis of MDD.
Vinnik and colleagues examined the effect of seasonality and BDNF polymorphism and levels on the depression outcome in dermatitis patients from onset through remission. Seasonally differential outcomes were observed in all groups. Their results suggest a strong influence of seasonality on depression outcome and BDNF expression.
Zalsman and associates investigated structural connectivity in a genetic rat model of depression. Using tractography-based analysis it emerged that the rat model of depression showed decreased connectivity in the corpus callosum and in the bilateral anterior commissure. Their findings in the rat model support findings in MDD patients, further suggesting that the vulnerability for developing depression is mainly polygenic and less likely to be due to childhood adversity.
Stojanovic et al., assessed executive functions (EF) in patients with treatment resistant depression before and after electroconvulsive therapy (ECT). Scores on depression rating scales significantly reduced over time with no negative effect on EF. It seems that ECT does not produce long-lasting EF deficits, nor does it exaggerate pre-existing ones. Improvement of EF performances during and after ECT induced improvement of mood symptoms is mostly based on reduction of time needed to plan problem solution.
In a brief report, Ulke and colleagues assessed the association between night-time sleep disturbances and brain arousal regulation the next day in depressed versus non-depressed elderly subjects. More sleep disturbances associated with a higher brain arousal the next day was detected in the depressed group. The results suggest that in people with depressive syndromes sleep disturbances are related to upregulation of brain arousal the following day, which is in line that dysregulation of brain arousal is a central pathophysiological aspect of depression.
Yours sincerely,
Siegfried Kasper
Chief Editor