Brain-Derived Neurotrophic Factor-5-HTTLPR Gene Interactions and Environmental Modifiers of Depression in Children

By P. S. Jensen. 2007

662 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/3c9fd01b5982875703302f448ebf273fda9c2edb

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Clinical Psychology

Citations in the corpus

The molecular neurobiology of depression (2008, neutral): “In addition, recent studies suggest complex interactions between the Bdnf G196A polymorphism, a polymorphism in the serotonin transporter gene, and stressful life event”
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).”
The Serotonin Transporter Promoter Variant (5-HTTLPR), Stress, and Depression Meta-Analysis Revisited: Evidence of Genetic Moderation (2011, background): “In fact, while 56 primary data studies have assessed whether 5-HTTLPR moderates the relationship between stress and depression, the Munafò et al(3) and Risch et al(4) metaanalyses included only 5 and 14 of those studies, respectively.(13-51) Further, Uher and McGuffin(11) have demonstrated that the ”
Altered connectivity in depression: GABA and glutamate neurotransmitter deficits and reversal by novel treatments (2019, background): “, 2007), and are at greater risk for depression when exposed to early life stress or trauma (Gatt et al., 2009; Kaufman et al., 2006; Kim et al., 2007).”
Research review: the neurobiology and genetics of maltreatment and adversity. (2010, background): “…been reported to drive individual differences in stress reactivity; for example, carrying two risk-associated gene variants may confer a greater level of vulnerability to stress reactivity compared to the combined risk conferred by each separately (e.g., Jabbi et al., 2007; Kaufman et al., 2006).”
Neurobiological and psychiatric consequences of child abuse and neglect. (2010, background): “Kaufman et al. (2006) hypothesized that a polymorphism (Val66Met polymorphism) in the BDNF gene might interact with the 5HTTLPR genotype to increase further the risk of depression in those with earlylife trauma.”