Meta-Analysis of the COMT Val158Met Polymorphism in Major Depressive Disorder: Effect of Ethnicity

Wang, Maiqiu; Ma, Yunlong; Yuan, Wenji; Su, Kunkai; Li, Ming D.

doi:10.1007/s11481-016-9651-3

Cited by 39 publications

(19 citation statements)

References 90 publications

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“…As hypothesized, the COMT and BDNF had main and interaction effects on WM. The positive effect of the COMT Val allele on cognitive abilities is consistent with previous research with Asian samples (Qian et al, 2009; Yeh et al, 2009; Wang et al, 2016), but opposite of previous findings from Western samples that COMT -Met carriers showed better cognitive performance in both patients (Bilder et al, 2002; Joober et al, 2002) and healthy individuals (Caldú et al, 2007; Sheldrick et al, 2008). The main effect of BDNF on WM was modest, yielding no significant post hoc contrasts.…”

Section: Discussionsupporting

confidence: 89%

“…Most studies that used Caucasian samples (Bruder et al, 2005; Aguilera et al, 2008) found that compared with the Val allele, the Met allele was correlated with better cognitive abilities, especially WM. On the other hand, in Asian samples, the Met allele was instead associated with higher incidence of major depressive disorder (MDD; Wang et al, 2016), lower IQ (Qian et al, 2009), lower scores on competency tests (Yeh et al, 2009), and lower WM (Wang et al, 2013). …”

Section: Introductionmentioning

confidence: 99%

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Interaction Effects of BDNF and COMT Genes on Resting-State Brain Activity and Working Memory

Chen

Xia

et al. 2016

Front. Hum. Neurosci.

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Catechol-O-methyltransferase (COMT) and brain-derived neurotrophic factor (BDNF) genes have been found to interactively influence working memory (WM) as well as brain activation during WM tasks. However, whether the two genes have interactive effects on resting-state activities of the brain and whether these spontaneous activations correlate with WM are still unknown. This study included behavioral data from WM tasks and genetic data (COMT rs4680 and BDNF Val66Met) from 417 healthy Chinese adults and resting-state fMRI data from 298 of them. Significant interactive effects of BDNF and COMT were found for WM performance as well as for resting-state regional homogeneity (ReHo) in WM-related brain areas, including the left medial frontal gyrus (lMeFG), left superior frontal gyrus (lSFG), right superior and medial frontal gyrus (rSMFG), right medial orbitofrontal gyrus (rMOFG), right middle frontal gyrus (rMFG), precuneus, bilateral superior temporal gyrus, left superior occipital gyrus, right middle occipital gyrus, and right inferior parietal lobule. Simple effects analyses showed that compared to other genotypes, subjects with COMT-VV/BDNF-VV had higher WM and lower ReHo in all five frontal brain areas. The results supported the hypothesis that COMT and BDNF polymorphisms influence WM performance and spontaneous brain activity (i.e., ReHo).

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Interaction Effects of BDNF and COMT Genes on Resting-State Brain Activity and Working Memory

Chen

Xia

et al. 2016

Front. Hum. Neurosci.

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“… showed in their study that the frequency of the Val allele among all healthy and depressed randomized European individuals was 51.42%. The allele frequency of COMT Val(108/158)Met, rs4680 genetic polymorphism is ethnicity‐dependent . Indeed, for the Asian ancestry, the Val allele had a frequency of 60.5% for the depressed population and 65.9% for the healthy population , whereas Hopkins et al .…”

Section: Discussionmentioning

confidence: 98%

The Catechol‐O‐methyltransferase Val(108/158)Met Genetic Polymorphism cannot be Recommended as a Biomarker for the Prediction of Venlafaxine Efficacy in Patients Treated in Psychiatric Settings

Tăranu

Asmar

Colle

et al. 2017

Basic Clin Pharma Tox

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The antidepressant venlafaxine is known to increase the turnover of cerebral monoamines, which are catabolized by the catechol-O-methyltransferase (COMT). The COMT (Val(108/158)Met, rs4680) genetic polymorphism affects the cerebral COMT activity. But whether this genetic polymorphism is associated with response to venlafaxine remains unclear. We assessed the impact of the COMT Val(108/158)Met, rs4680 genetic polymorphism on the efficacy of venlafaxine in depressed patients. This study was nested in the METADAP cohort, a real-world naturalistic treatment study in psychiatric settings. A total of 206 Caucasian patients with a unipolar major depressive episode (DSM-IVTR) treated with venlafaxine and evaluated with the Hamilton Depression Rating Scale (HDRS) were studied. One hundred and eighty patients were genotyped for the COMT Val(108/158)Met, rs4680 genetic polymorphism and classified into three genotype subgroups: Val/Val, Val/Met and Met/Met. The COMT genotype was the explanatory variable, and the variables to be explained were HDRS score, HDRS score improvement over time, response rate and remission rate. Venlafaxine had a trend to higher efficacy in the Val/Val patients as compared to Met/Met carriers, as shown by the HDRS score improvement after 3 months of treatment, but this result was not significant in mixed models [Val/Val: 59.78% (±22.4); Val/Met: 51.64% (±26.3); Met/Met: 39.52% (±27.6)]. The percentage of responders and remitters after 3 months of treatment was not significantly different in the three genotype groups, although coherent trends were shown. The COMT Val(108/158)Met, rs4680 genetic polymorphism cannot be recommended as a biomarker for the prediction of venlafaxine efficacy in patients treated in psychiatric settings.

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“…60% of the metabolic degradation of dopamine (Karoum et al 1994), a neurotransmitter which plays a role in antidepressant action (Porcelli et al 2011). Moreover, Comt polymorphisms have been associated with depression (Koike et al 2018; Wang et al 2016) and response to antidepressants (Antypa et al 2013; O’Leary et al 2014). Adora1 encodes A 1 receptor, whose antagonism mediates caffeine-induced wakefulness (Fredholm et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Withdrawal of caffeine after its chronic administration modifies the antidepressant-like activity of atypical antidepressants in mice. Changes in cortical expression of Comt, Slc6a15 and Adora1 genes

et al. 2018

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RationaleDepressed patients often present increased consumption of caffeine.ObjectivesWe aimed to investigate the effects of chronic treatment with caffeine (5 mg/kg, twice daily for 14 days) on the activity of single, ineffective doses of agomelatine (20 mg/kg) or mianserin (10 mg/kg) given on day 15 alone or simultaneously with caffeine.MethodsWe used the forced swim test (FST), tail suspension test (TST), and locomotor activity test in mice and quantitative real-time PCR analysis of the selected genes in the cerebral cortex (Cx).ResultsThere were no changes in the immobility time between mice that received saline and caffeine for 14 days. Administration of agomelatine or mianserin on day 15 did not produce an antidepressant-like effect, but such effect was observed after administration of agomelatine or mianserin simultaneously with caffeine on day 15, in both mice that received saline and caffeine for 14 days. In mice treated with caffeine for 14 days, joint administration of agomelatine or mianserin and caffeine on day 15 decreased solute carrier family 6, member 15 (Slc6a15), messenger RNA (mRNA) level in the Cx, compared to the group which received only the respective antidepressant on this day. Moreover, in mice treated with caffeine for 14 days, joint administration of mianserin and caffeine on day 15 decreased adenosine A1 receptor (Adora1) and catechol-O-methyltransferase (Comt) mRNA level in the Cx, compared to the group which received mianserin without caffeine on this day.ConclusionsWithdrawal of caffeine after its chronic intake can modify the activity of antidepressants. Adora1, Slc6a15, and Comt may be involved in the antidepressant-like effect observed after joint administration of caffeine and mianserin or agomelatine, following chronic treatment with caffeine.

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Meta-Analysis of the COMT Val158Met Polymorphism in Major Depressive Disorder: Effect of Ethnicity

Cited by 39 publications

References 90 publications

Interaction Effects of BDNF and COMT Genes on Resting-State Brain Activity and Working Memory

Interaction Effects of BDNF and COMT Genes on Resting-State Brain Activity and Working Memory

The Catechol‐O‐methyltransferase Val(108/158)Met Genetic Polymorphism cannot be Recommended as a Biomarker for the Prediction of Venlafaxine Efficacy in Patients Treated in Psychiatric Settings

Withdrawal of caffeine after its chronic administration modifies the antidepressant-like activity of atypical antidepressants in mice. Changes in cortical expression of Comt, Slc6a15 and Adora1 genes

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