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Review
. 2015 Apr 8;16(4):7796-801.
doi: 10.3390/ijms16047796.

Inflammatory biomarkers as differential predictors of antidepressant response

Kenji Hashimoto  1
Affiliations
Review

Inflammatory biomarkers as differential predictors of antidepressant response

Kenji Hashimoto. Int J Mol Sci. .

Abstract

Although antidepressants are generally effective in the treatment of major depressive disorder (MDD), it can still take weeks before patients feel the full antidepressant effects. Despite the efficacy of standard treatments, approximately two-thirds of patients with MDD fail to respond to pharmacotherapy. Therefore, the identification of blood biomarkers that can predict the treatment response to antidepressants would be highly useful in order to improve this situation. This article discusses inflammatory molecules as predictive biomarkers for antidepressant responses to several classes of antidepressants, including the N-methyl-d-aspartate (NMDA) receptor antagonist ketamine.

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Figures

Figure 1
Figure 1
The balance between Th1 (cellular) and Th2 (humoral) response to the adaptive immune system. The immune system, composed of Th1-mediated cellular immunity and Th2-mediated humoral immunity, is essential to maintain health. Both Th1 and Th2 immunity are tightly controlled, but abnormalaties of the “immune balance” between Th1 and Th2 immunity is implicated in the pathophysiology of MDD. Th2 shift causes inflammation and increase in CRP protein and pro-inflammatory cytokines (e.g., IL-6), resulting in depressive symptom. Th1 shift also causes depressive symptom. 5-HT and NE are known to confer differential effects on inflammation. 5-HT and NE mediate a Th1 shift and a Th2 shift, respectively. Furthermore, 5-HT inhibits the production of Th2 cytokines such as IL-6, whereas NE inhibits production of Th1 pro-inflammatory cytokines, including TNF-α [18]. The SSRIs (e.g., paroxetine, sertraline, fluoxetine, escitalopram) cause a Th1 shift. The SNRIs (venlafaxine, duloxetine), and NRIs (nortriptyline, reboxetine) cause a Th2 shift [18]. Bupropion and mirtazapine may induce Th2 and Th1 shift, respectively [18]. In addition, the NMDA receptor antagonist ketamine may cause a Th2 shift. Thus, the regulation of the “immune balance” between Th1 and Th2 immunity is critical for therapy of MDD.
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