The interaction of stressful life events and a serotonin transporter polymorphism in the prediction of episodes of major depression: a replication.
By Kenneth S. Kendler, Jonathan W Kuhn, J. Vittum, C. Prescott, B. Riley. Archives of General Psychiatry, 2005
645 citations recorded by the source corpus.
Subfields: Behavioral Neuroscience, Biological Psychiatry, Cellular and Molecular Neuroscience
View Paper: https://www.semanticscholar.org/paper/25cd1c94261c02849126892c64b2a90551c5b46a
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Behavioral Neuroscience
- Michael Rutter
- Terrie E. Moffitt
- Avshalom Caspi
- A. Beck
- Bruce S. McEwen
- M. Enoch
- Keith Bredemeier
- Katja Wiech
In Biological Psychiatry
In Cellular and Molecular Neuroscience
- A. Beck
- Terrie E. Moffitt
- Avshalom Caspi
- Michael Rutter
- Marcus Munafò
- Sarah Marie Brown
- Ahmad R. Hariri
- Dennis S. Charney
Citations in the corpus
- Practice parameter for the assessment and treatment of children and adolescents with depressive disorders. (2007, background): “…and twin studies have shown that MDD is a familial disorder, which is caused by the interaction of genetic and environmental factors (Birmaher et al., 1996; Caspi et al., 2003; Kendler et al., 2005; Pilowsky et al., 2006; Pine et al., 1998; Reinherz et al., 2003; Weissman et al., 2005, 2006b).”
- Serotonin transporter (5-HTTLPR) genotype and amygdala activation: a meta-analysis. (2008, background): “Moreover, the 5-HTTLPR S allele has been associated with relatively increased risk for depression in the context of environmental adversity (12-15), a relationship that may be mediated by increased neuroticism (16), a psychometrically robust index of trait negative affect.”
- Strategy for investigating interactions between measured genes and measured environments. (2005, neutral): “Genotype was statistically unrelated to outcomes in the full cohorts of these studies; genotypes’ effects on disorder, apart from their role in the GxE, were virtually nil and statistically undetectable.(8-12,15,22,28,125) In these studies, genotype effects were only revealed among individuals expos”
- The Serotonin Transporter Promoter Variant (5-HTTLPR), Stress, and Depression Meta-Analysis Revisited: Evidence of Genetic Moderation (2011, background): “Interestingly, 3 studies have explicitly looked at both acute and chronic stressors in their cohorts and all 3 have found that the evidence for moderating effects was stronger for chronic stressors.(13,19,48) In addition to the type of stressor studied, the stress assessment method used by investiga”
- Interaction Between the Serotonin Transporter Gene (5-HTTLPR), Stressful Life Events, and Risk of Depression (2009, background): “Chipman et al,16 2007 2095 (1089) 23 (20-24) 33 46 21 Cross sectional No List of Threatening Eventsb Depression rating scale Failed to replicate”
- The evolution of the cognitive model of depression and its neurobiological correlates. (2008, background): “Also, in some studies, adverse experiences, for example, abuse in childhood (28), appear to represent a distal predisposition to depression, whereas in others, 5-HTTLPR genotype moderates the depressogenic effects of more proximal events (11).”