ArticleEuropean archives of psychiatry and clinical neuroscience2014
Interaction among childhood trauma and functional polymorphisms in the serotonin pathway moderate the risk of depressive disorders.
Article in European archives of psychiatry and clinical neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- Vitamin D moderates the interaction between 5-HTTLPR and childhood abuse in depressive disorders.Scientific reports · 2020Trial
- Interaction between childhood trauma experience and TPH2 rs7305115 gene polymorphism in brain gray matter volume.Behavioral and brain functions : BBF · 2023Article
- Genetic architecture of well-being: cumulative effect of serotonergic polymorphisms.Social cognitive and affective neuroscience · 2023Article
- Molecular Biomarkers Predictive of Sertraline Treatment Response in Young Children With Autism Spectrum Disorder.Frontiers in genetics · 2020Article
- Gene-Environment Interactions in Psychiatry: Recent Evidence and Clinical Implications.Current psychiatry reports · 2019Review
- Genome-wide gene-environment interaction in depression: A systematic evaluation of candidate genes: The childhood trauma working-group of PGC-MDD.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2018Article
- TPH-2 Gene Polymorphism in Major Depressive Disorder Patients With Early-Wakening Symptom.Frontiers in neuroscience · 2018Article
- Selected issues of the DGPPN Congress in 2013.European archives of psychiatry and clinical neuroscience · 2014Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depressive disorders are influenced by a complex interplay between genetic and environmental factors. Multiple studies support a role of serotonergic pathways in the pathophysiology of depressive disorders. As a rate-limiting enzyme of serotonin synthesis in the brain, tryptophan hydroxylase 2 (TPH2) represents a plausible candidate gene. This also applies to the serotonin reuptake transporter (5-HTTLPR) regulating the availability of serotonin in the synaptic gap. We hypothesize that functional polymorphisms (TPH2: rs7305115, 5-HTTLPR and rs25531) within both genes contribute to the risk of depressive disorders after childhood abuse in adult life. To confirm our results, we investigated two independent samples of Caucasian subjects from the study of health in Pomerania (SHIP-LEGEND: n = 2,029 and SHIP-TREND-0: n = 2,475). Depression severity was assessed by the Beck depression inventory (BDI-II) for LEGEND and the patient health questionnaire (PHQ-9) for TREND-0. Childhood abuse was assessed by the childhood trauma questionnaire. Rs7305115 (TPH2) revealed significant effects in SNP × abuse and SNP × SNP as well as in the three-way interaction. This three-way interaction among abuse, TPH2 and 5-HTTLPR showed a significant effect on depression score (p = 0.023). The SS genotype of 5-HTTLPR was associated with increased depression scores after childhood abuse only in carriers of the low-expression TPH2 GG genotype, whereas the TPH2 AA genotype reversed this effect. Our results support the role of interaction effects of genetic variants within serotonergic pathways. Genetic variants that may decrease the presynaptic serotonin concentration were associated with increased adult depressive symptoms in subjects with childhood abuse.
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