The role of selective serotonin reuptake inhibitors in preventing relapse of major depressive disorder

Abstract

The objective of this review was to evaluate the efficacy of selective serotonin reuptake inhibitors (SSRIs) and SSRIs compared with other treatment modalities in preventing relapse after an episode of major depressive disorder (MDD). An Ovid MEDLINE and PsycINFO search (from 1987 to August 2017) was conducted using the following terms: selective serotonin reuptake inhibitors, antidepressants, depression, prevention, prophylaxis, relapse and MDD. Using predefined criteria, two authors independently selected and reached consensus on the included studies. Sixteen articles met the criteria: 10 compared the relapse rate of selective SSRIs with placebo or other SSRIs; one discussed the effectiveness of SSRIs plus psychotherapy, two compared SSRI tricyclic antidepressants (TCAs), two were mainly composed of TCAs plus psychotherapy, and one compared SSRIs and serotonin norepinephrine reuptake inhibitors (SNRIs). According to the included studies, the relapse risk in adults was lower when SSRIs were combined with psychotherapy. Results comparing SSRIs and SNRIs were inconclusive. TCAs may be equally as effective as SSRIs. Atypical antidepressants (mirtazapine and St John's Wort) had no significant difference in efficacy and remission rates compared with SSRIs. Escitalopram appeared to fare better in efficacy than other SSRIs, owing to a higher prophylactic efficacy and lower side effects; however, according to the current data, this difference was not significant. To conclude, this review provides evidence that continuing SSRIs for 1 year reduces risk of MDD and relapse. Furthermore, the combination of SSRIs and cognitive behavioural therapy may effectively reduce relapse. Escitalopram appeared to yield better results and fewer side effects than did other SSRIs or SNRIs. The effectiveness in reducing relapse of SSRIs was similar to that of TCAs and atypical antidepressants.

Lipopolysaccharide-Induced Depression-Like Behaviors Is Ameliorated by Sodium Butyrate via Inhibiting Neuroinflammation and Oxido-Nitrosative Stress

“…The experimental mice with or without LPS and/or SB treatment were divided into 8 groups (n = 10/group): group I was treated with vehicle (dimethyl sulfoxide [DMSO]:PBS [1: 1]) of SB for 10 consecutive days, and then treated with saline 30 min after the last vehicle injection; group II, III and IV were treated with 20 mg/ kg of fluoxetine (DMSO:PBS [ for 10 consecutive days, respectively, and then treated with saline 30 min after the last drug injection; group V was treated with vehicle (DMSO:PBS [1: 1]) of SB for 10 consecutive days, and then treated with 0.83 mg/kg of LPS 30 min after the last vehicle injection; this dosage of LPS was selected according to our previous studies [6,7]; group VI was treated with 20 mg/kg of fluoxetine for 10 consecutive days, and then treated with LPS (0.83 mg/kg) 30 min after the last fluoxetine injection; group VII was treated with 100 mg/kg of SB for 10 consecutive days, and then treated with LPS (0.83 mg/kg) 30 min after the last SB injection; and group VIII was treated with 300 mg/kg of SB for 10 consecutive days, and then treated with LPS (0.83 mg/kg) 30 min after the last SB injection. The timeline for the tail suspension test (TST), forced swim test (FST), sucrose preference test (SPT), open field test (OFT), and biochemical assays were outlined in Figure 1.…”

“…Its pathogenesis has been well documented in the previous studies [1] and has been confirmed to be associated with repeated exposure to harmful stress, which may include a variety of social and un-social stimuli, such as poor parental care [2], drug addiction [3], and heart surgery [4]. The presently available antidepressants in clinic, such as the selective monoamine oxidase inhibitors and the serotonin reuptake inhibitors, ameliorate depressive symptoms mainly through rectifying the monoamine dysfunction in the brain [5][6][7]. However, during the clinical application these agents exhibit numerous side effects [8], and only one third of patients acquire effective responses to these antidepressants [9].…”

Kynurenic acid is a potential overlapped biomarker between diagnosis and treatment response for depression from metabolome analysis

“…Selective serotonin reuptake inhibitors (SSRIs) are commonly used as first-line treatment for MDD 3 . They are thought to increase the extracellular availability of the neurotransmitter serotonin by limiting its reabsorption into presynaptic cells, increasing serotonin levels in the synaptic cleft, and making it available for postsynaptic receptor binding 4 .…”

The Changes of Gut Microbiota in Drug-Naïve First-Episode MDD Patients Under Treatment by SSRIs

“…[3] However, the slow effect and relapse, leading to long-term and reduplicated uses, create a severe disadvantage for patients and even build the barriers for SSRIs applications. [4,5] Therefore, it suggests to further reveal the underlying mechanisms in details other than simply descriptions of decreased 5-HT in the occurrence of MDD.…”