The present study aimed to explore whether 4 single nucleotide polymorphisms (SNPs) within the AHI1 gene could be associated with major depressive disorder (MD) and bipolar disorder (BD), and whether they could predict clinical outcomes in mood disorders.

We tried to review and update clinical and preclinical studies evaluating vilazodone's role as an antidepressant for patients with major depressive disorder (MDD). In terms of its mechanism of actions, we sought to elaborate them mainly through preclinical animal studies. A data search was conducted in November 1, 2013, using the key terms "vilazodone" or "Viibryd," in PubMed and Medline databases. All published and unpublished studies are included and citations from publications were also reviewed for additional references. Five unpublished, phase-II and two pivotal published phase-III clinical trials with nearly identical design (8-week, double-blind, randomized, and placebo-controlled) investigated efficacy of vilazodone, were found for the treatment of patients with MDD. Two post-hoc studies and one long-term open study were also included. Data were thoroughly reviewed to incorporate the pharmacology, action mechanism, efficacy and safety for the vilazodone in the treatment of major depressive disorder. Vilazodone is an antidepressant with novel mechanism of action because its chemical structure is unrelated to conventional antidepressant, and it has a selective serotonin (5-HT) reuptake inhibitor and 5-HT1A receptor partial agonist profile. Vilazodone is an effective and safe treatment option with its novel action mechanisms for patients with depression. Its putative benefits compared with other antidepressants must be thoroughly studied in adequately-powered and well-designed future clinical trials.

A relevant part of the social and personal burden caused by Bipolar Disorder (BD) is related to depressive phases. Authors investigated the genetic impact of a set of variations located in CRY1, a gene involved in the control of the circadian rhythms, towards depressive episodes in a sample of bipolar patients from the STEP-BD sample. As a secondary analysis, CYR1 variations were analyzed as predictors of sleep disruption.

The aim of the present work is to investigate the existence of epistatic interactions possibly influencing psychotropic agents' response between rs6740584 within Cyclic adenosine monophosphate Response Element Binding (CREB) and rs12775799 within cAMP response element-modulator (CREM) variants in bipolar disorder (BD) and major depressive disorder (MDD). All BD and MDD patients were administered with the Young Mania Rating Scale (YMRS) and Hamilton Depression Rating Scale (HAMD) at baseline and at endpoint, respectively. A multiple regression model was employed to investigate the existence of possible epistatic interactions between the two variants and diverse clinical factors including drug response in affective disorders. No significant epistatic interaction was observed between rs6740584 within CREB and rs12775799 within CREM on both symptom improvement and other clinical factors in affective disorders. Our preliminary results suggest that no epistatic interaction between rs6740584 within CREB and rs12775799 within CREM should exist on clinical improvement and clinical factors in affective disorders.

This study aimed to compare the efficacy and safety of escitalopram, vortioxetine, and desvenlafaxine for acute treatment of major depressive disorder (MDD) with cognitive complaint (CC).

Gene variants within the serotonin pathway have been associated with major depressive disorder (MDD) treatment outcomes, however a possible different modulation on pharmacological or psychological treatments has never been investigated.