scholarly journals Interactions Between Glycogen Synthase Kinase-3β Gene Polymorphisms, Negative Life Events, and Susceptibility to Major Depressive Disorder in a Chinese Population

2021 ◽  
Vol 11 ◽  
Author(s):  
Jiarun Yang ◽  
Siyuan Ke ◽  
Zhengxue Qiao ◽  
Xiuxian Yang ◽  
Xiaohui Qiu ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Life Events ◽  
Glycogen Synthase ◽  
Allelic Variation ◽  
Negative Life Events ◽  
Glycogen Synthase Kinase ◽  
Environment Interaction ◽  
Major Depressive ◽  
Gsk 3Β

Background: Recent studies suggest that glycogen synthase kinase (GSK)-3β is involved in the development of major depressive disorder (MDD). The aim of this study was to investigate the interaction between GSK-3β polymorphism (rs6438552, rs334558, and rs2199503) and negative life events in the pathogenesis of major depressive disorder (MDD).Methods: DNA genotyping was performed on peripheral blood leukocytes in 550 patients with MDD and 552 age- and gender-matched controls. The frequency and severity of negative life events were assessed by the Life Events Scale (LES). A chi-square method was employed to assess the gene-environment interaction (G × E).Results: Differences in rs6438552, rs334558, and rs2199503 genotype distributions were observed between MDD patients and controls. Significant G × E interactions between allelic variation of rs6438552, rs334558, and rs2199503 and negative life events were observed. Individuals with negative life events and carrying genotypes of rs6438552 A+, rs334558 A+, and rs2199503G+ have increased the risk of depression.Conclusions: These results indicate that interactions between the GSK-3β rs6438552, rs334558, and rs2199503 polymorphisms and environment increases the risk of developing MDD.

Increased prevalence of negative life events in subtypes of major depressive disorder

2001 ◽  
Vol 42 (1) ◽  
pp. 57-63 ◽  
Author(s):  
Yoav Kohn ◽  
Joseph Zislin ◽  
Ofer Agid ◽  
Bella Hanin ◽  
Tristan Troudart ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Life Events ◽  
Negative Life Events ◽  
Major Depressive

The association of suicide risk with negative life events and social support according to gender in Asian patients with major depressive disorder

2015 ◽  
Vol 228 (3) ◽  
pp. 277-282 ◽  
Author(s):  
Subin Park ◽  
Ahmad Hatim Sulaiman ◽  
Manit Srisurapanont ◽  
Sung-man Chang ◽  
Chia-Yih Liu ◽  
...  
Keyword(s):  
Social Support ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Life Events ◽  
Suicide Risk ◽  
Negative Life Events ◽  
Major Depressive ◽  
Asian Patients

Excessive activation of the loop between the NR2B subunit of the N-methyl-d-aspartate receptor and glycogen synthase kinase-3β in the hippocampi of patients with major depressive disorder

2012 ◽  
Vol 24 (1) ◽  
pp. 26-33 ◽  
Author(s):  
Dong Hoon Oh ◽  
Seon-Cheol Park ◽  
Yong Chon Park ◽  
Seok Hyeon Kim
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Animal Studies ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Data Sets ◽  
Major Depressive ◽  
Expression Levels ◽  
Nitric Oxide Synthase 1 ◽  
Excessive Activation

Objective: We showed previously that glycogen synthase kinase-3β (GSK-3β) levels are significantly elevated in the hippocampi of patients with major depressive disorder (MDD). However, the exact cause of this elevation and its function are unknown. Recent animal studies have suggested a mechanism involving the N-methyl-d-aspartate (NMDA) NR2B–GSK-3β loop.Methods: To investigate the existence of an NR2B–GSK-3β loop in the hippocampi of patients with MDD, we examined the expression of NR2B. We also attempted to identify markers that correlate with NR2B levels in the hippocampus, using the Stanley Neuropathology Consortium Integrative Database (SNCID). The SNCID is a web-based tool used to integrate Stanley Medical Research Institute (SMRI) data sets.Results: We found that hippocampal levels of NR2B and DLGAP1 mRNA were higher in the MDD group (n = 8) than in unaffected controls (n = 12) (p < 0.05). NR2B expression levels were correlated with the expression levels of NR2A, NR1, DLGAP1, GSK-3β and nitric oxide synthase 1, as well as with the number of calretinin-immunoreactive neurons in the hippocampus in all subjects in the SNC (n = 42, p < 0.001).Conclusion: The results of our study show the possible involvement of excessive activation of the NR2B–GSK-3β loop in the overexpression of GSK-3β in the hippocampi of patients with MDD.

scholarly journals The death(s) of close friends and family moderate genetic influences on symptoms of major depressive disorder in adolescents

2010 ◽  
Vol 41 (4) ◽  
pp. 721-729 ◽  
Author(s):  
S. Gheyara ◽  
K. L. Klump ◽  
M. McGue ◽  
W. G. Iacono ◽  
S. A. Burt
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Life Events ◽  
Negative Life Events ◽  
Genetic Influences ◽  
Phenotypic Variance ◽  
Major Depressive ◽  
Sibling Interaction ◽  
Behavior Study ◽  
Gene Environment

BackgroundPrior work has suggested that genetic influences on major depressive disorder (MDD) may be activated by the experience of negative life events. However, it is unclear whether these results persist when controlling for the possibility of confounding active gene–environment correlations (rGE).MethodWe examined a sample of 1230 adopted and biological siblings between the ages of 10 and 20 years from the Sibling Interaction and Behavior Study. MDD was measured via a lifetime DSM-IV symptom count. Number of deaths experienced served as our environmental risk experience. Because this variable is largely independent of the individual's choices/behaviors, we were able to examine gene–environment interactions while circumventing possible rGE confounds.ResultsBiometric analyses revealed pronounced linear increases in the magnitude of genetic influences on symptoms of MDD with the number of deaths experienced, such that genetic influences were estimated to be near-zero for those who had experienced no deaths but were quite large in those who had experienced two or more deaths (i.e. accounting for roughly two-thirds of the phenotypic variance). By contrast, shared and non-shared environmental influences on symptoms of MDD were not meaningfully moderated by the number of deaths experienced.ConclusionsSuch results constructively replicate prior findings of genetic moderation of depressive symptoms by negative life events, thereby suggesting that this effect is not a function of active rGE confounds. Our findings are thus consistent with the notion that exposure to specific negative life events may serve to activate genetic risk for depression during adolescence.

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