Evidence for an association between a G-protein-β3-gene variant with depression and response to antidepressant treatment

Zill, Peter; Baghai, Thomas C.; Zwanzger, Peter; Schüle, Cornelius; Minov, Christo; Rupprecht, Rainer; Riedel, Michael; Neumeier, K.; Bondy, Brigitta

doi:10.1016/s0924-977x(00)80216-3

Cited by 39 publications

(59 citation statements)

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“…Moreover, a significant association between TT homozygosity and response to antidepressant treatment after 4 weeks was observed. Thus, the G-protein b3 subunit appears to be a susceptibility factor for major depression (Zill et al, 2000). In a Korean sample, significantly more carriers of the 825T allele were found in major depressive disorder patients than in normal controls ).…”

Section: G-proteinsmentioning

confidence: 94%

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Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

227

126

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Biological markers for depression are of great interest to aid in elucidating the causes of major depression. We assess currently available biological markers to query their validity for aiding in the diagnosis of major depression. We specifically focus on neurotrophic factors, serotonergic markers, biochemical markers, immunological markers, neuroimaging, neurophysiological findings, and neuropsychological markers. We delineate the most robust biological markers of major depression. These include decreased platelet imipramine binding, decreased 5-HT1A receptor expression, increase of soluble interleukin-2 receptor and interleukin-6 in serum, decreased brain-derived neurotrophic factor in serum, hypocholesterolemia, low blood folate levels, and impaired suppression of the dexamethasone suppression test. To date, however, none of these markers are sufficiently specific to contribute to the diagnosis of major depression. Thus, with regard to new diagnostic manuals such as DSM-V and ICD-11 which are currently assessing whether biological markers may be included in diagnostic criteria, no biological markers for major depression are currently available for inclusion in the diagnostic criteria.

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Section: G-proteinsmentioning

confidence: 94%

“…Abnormal signal transduction pathways have been implicated in the pathogenesis of major depression and bipolar disorder (Zill et al 2000). G-proteins are key elements of these pathways in the regulation of cellular responses by transmission of signals from receptors to effector proteins.…”

Section: G-proteinsmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

227

126

View full text Add to dashboard Cite

show abstract

“…The Gb3s variant has been reported to be not only associated with increased signal transduction and ion transport, but also with pathophysiological conditions such as hypertension [3][4][5][6][7] and obesity. 8,9 More recently, Zill et al 10 found an association between the C825T SNP of GNB3 and depression. They reported that the frequency of the T allele was significantly higher in depressive patients than in healthy controls and schizophrenic patients.…”

Section: Introductionmentioning

confidence: 99%

Association between a G-protein β3 subunit gene polymorphism and the symptomatology and treatment responses of major depressive disorders

et al. 2003

Pharmacogenomics J

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The genes involved in signal transduction are major candidates in association studies on affective disorders and responses to antidepressants. We investigated whether the C825T polymorphism of the b3 subunit of G protein (GNB3) gene is associated with the symptom severity or treatment response of major depressive disorders (MDDs) in a Korean sample of 106 MDD patients; our study also included 133 healthy controls. Hypertensive subjects were excluded from the study because association between GNB3 variants and hypertension has been reported in previous studies. We found significantly more carriers of the 825T allele in MDD patients than in normal controls (w 2 ¼ 6.37, P ¼ 0.012; OR ¼ 2.19, 95% CI 1.18-4.05). The T-allele carriers showed higher scores than those with the CC genotype in the baseline total and in some subcategories of the Hamilton Depression Rating Scale (Po0.05). We also found a statistically significant association between T-allele carriers and antidepressant treatment response (Po0.05). These results suggest that the T allele of the C825T polymorphism in the GNB3 gene is associated with MDD. It was also demonstrated that MDD patients bearing the T allele had a severe symptomatology and a better response to antidepressant treatment than patients without the T allele.

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“…Due to their pivotal function in many cell types, variation in the genes encoding the subunits of G proteins has the potential to play a role in numerous clinical conditions. Specifically, investigators have studied possible associations of the frequent substitution of a C with a T nucleotide at position 825 in exon 10 in the gene encoding the G protein β3 subunit (GNB3), resulting in the silent Ser275Ser polymorphism, with hypertension [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] and related cardiovascular phenotypes [16][17][18][19][20][21][22], and with obesity [22][23][24][25], psychological syndromes [26][27][28], type 1 diabetes complications (nephropathy, retinopathy and neuropathy) [29,30], type 2 diabetes [13,22,31,32], cancer [33] and various immunological responses [34]. The 825C>T polymorphism is associated with the occurrence of a splice variant with an in-frame deletion of 41 amino acids (from exon 9) including the fourth of seven Trp-Asp repeats, each consisting of approximately 40 highly conserved amino acids, which normally form a β-propeller peptide structure [1].…”

Section: Introductionmentioning

confidence: 99%

Studies of the association of the GNB3 825C>T polymorphism with components of the metabolic syndrome in white Danes

et al. 2005

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Aims/hypothesis: The 825C>T polymorphism in the gene encoding the G protein β3 subunit (GNB3) causes enhanced G protein activation and increased in vitro cell proliferation. This polymorphism is also repeatedly associated with an increased risk of hypertension and has been studied in relation to obesity with divergent results. Only a few association studies have investigated whether this polymorphism is related to type 2 diabetes or the metabolic syndrome. We estimated the impact of the GNB3 825C>T polymorphism in relatively large-scale association studies of common phenotypes of the metabolic syndrome. Materials and methods: The GNB3 825C>T polymorphism was genotyped in 7,518 white Danish subjects using mass spectrometry analysis of PCR products. Case-control studies were undertaken for obesity, hypertension, type 2 diabetes and the metabolic syndrome, and a meta-analysis including data from the present study and previous studies of hypertension was performed. Quantitative trait studies of metabolic variables were carried out in 4,387 glucose-tolerant subjects. Results: We observed minor differences in 825C>T genotype distributions for type 2 diabetes (CC/CT/TT 49/41/10% (control) vs 46/46/9% (cases), respectively, p=0.007); however, after correction for multiple testing, these were not statistically significant. No association was found with hypertension, obesity or the metabolic syndrome. Curiously, the T allele was associated with nominally lower systolic and diastolic blood pressure levels-a finding in contrast with most previous studies-but not with other metabolic variables. Meta-analysis demonstrated a high degree of heterogeneity between study populations of different ethnic origin. Although there was a tendency towards an increased risk of hypertension among 825T allele carriers, this was not statistically significant. Conclusions/interpretation: The present study suggests no major involvement of the GNB3 825C>T polymorphism in components of the metabolic syndrome.

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Evidence for an association between a G-protein-β3-gene variant with depression and response to antidepressant treatment

Cited by 39 publications

References 0 publications

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Association between a G-protein β3 subunit gene polymorphism and the symptomatology and treatment responses of major depressive disorders

Studies of the association of the GNB3 825C>T polymorphism with components of the metabolic syndrome in white Danes

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