Dear colleagues,
It is my great pleasure to introduce to you the fifth issue of 2018 featuring original research on treatment options and efficacy as well as biomarkers in depression.
Dodd et al., review recommendations designed to ensure safety for patients with major depression and to aid in monitoring and management of adverse events during antidepressant treatment. Risk factors for pharmacotherapy vary between individual patients thus proper risk assessment prior to pharmacotherapy in addition to safety monitoring during pharmacotherapy is necessary in order to mitigate adverse events and to optimise benefits of treatment.
Lima-Ojeda and colleagues review the neurobiology of depression. Depression is a complex disorder that involves structural and functional changes from early development. In those who are at genetic risk for depression, early stress factor can mediate the gene expression in addition to the genetic risk. Furthermore, evidence suggests that early endocrine and immune interactions have an important impact on monoamine function.
Colle and associates investigated whether hippocampal volumes predict response to antidepressant treatment in patients with major depressive disorder. They found that non-responders had smaller hippocampal volume at baseline in comparison to those who achieved remission. The authors conclude that smaller hippocampal volumes predict lower response rates in antidepressant treated patients.
Chang and associates investigated the heart rate variability (HRV) in unmedicated patients with major depressive disorder and the changes after treatment with agomelatine or combination treatment. They found a significant increase in high frequency (HF) HRV after agomelatine monotherapy, decrease in low-frequency (LF) HRV and HF-HRV as well as an increase in LF/HF ratio after combination therapy. To conclude, clinicians should consider HRV effects when adding sedative-hypnotics to agomelatine therapy.
Kranaster et al., assessed the effects of electroconvulsive therapy (ECT) treatment on immune markers in the cerebrospinal fluid (CSF) in patients with depression. It emerged that higher CSF levels indicating increased macrophage/microglia activation at baseline predicted a better treatment response to ECT. Their results that macrophages/microglia are involved in the pathophysiology of depression and that the efficacy of ECT may partly be explained by modulation of the immune system within the brain.
Rossetti and colleagues made a genome-wide analysis to assess the immune-regulatory activity of the antidepressant agomelatine in response to an inflammatory challenge. Administration of lipopolysaccharide (LPS) induced transcription of several genes associated with immune and inflammatory pathways. Agomelatine modulated pathways related to antidepressant activity and was able to prevent the activation of genes induced by LPS. These results bring about the association between depression and inflammation, potentially revealing new targets for pharmacological treatment for depression associated with inflammation.
In a brief report, Caldieraro et al., examined the association of a Val66Met polymorphism with serum levels of BDNF and inflammatory markers among patients with depression. Met allele carriers were found to have higher BDNF and lower TNF-α. Low BDNF and high inflammation in major depression may be influenced by the Val66Met polymorphism as the results suggest.
Yours sincerely