Abstract
Disturbances of brain derived neurotrophic factor (BDNF) signalling have been implicated in the evolution of depression, which likely arises, in part, as a result of diminished synaptic plasticity. Predictably, given stressor involvement in depression, BDNF is affected by recent stressors as well as stressors such as neglect experienced in early life. The effects of early life maltreatment in altering BDNF signalling may be particularly apparent among those individuals with specific BDNF polymorphisms. We examined whether polymorphisms of the Val66Met genotype might be influential in moderating how early-life events play out with respect to later coping styles, cognitive flexibility and depressive features. Among male and female undergraduate students (N = 124), childhood neglect was highly related to subsequent depressive symptoms. This outcome was moderated by the BDNF polymorphism in the sense that depressive symptoms appeared higher in Met carriers who reported low levels of neglect than in those with the Val/Val allele. However, under conditions of high neglect depressive symptoms only increased in the Val/Val individuals. In effect, the Met polymorphism was associated with depressive features, but did not interact with early life neglect in predicting later depressive features. It was further observed that among the Val/Val individuals, the relationship between neglect and depression was mediated by emotion-focused styles and diminished perceived control, whereas this mediation was not apparent in Met carriers. In contrast to the more typical view regarding this polymorphism, the data are consistent with the perspective that in the presence of synaptic plasticity presumably associated with the Val/Val genotype, neglect allows for the emergence of specific appraisal and coping styles, which are tied to depression. In the case of the reduced degree of neuroplasticity expected in the Met carriers, early life adverse experiences are not tied to coping styles, and hence less likely to be translated into depressive states.
Highlights
Increasing attention has been devoted to the possibility that growth factors, such as brain derived neurotrophic factor (BDNF), through actions on neurogenesis and neuroplasticity, contribute to the evolution of depressive disorders [1]
Alternative models in which BDNF genotype moderated the path between perceived control and depressive scores were not significant. Both depression and the Val66Met polymorphism have been associated with deficits in neurotrophic support [12,48,49], reduced size and function of the hippocampus and prefrontal cortex [50,51,52,53], as well as use of a ruminative coping style [37,38], the Val66Met polymorphism was not necessarily linked to the appearance of depression [54,55,56]
As indicated earlier, the findings concerning the relationship between BDNF polymorphisms and depression have been inconsistent, and the suggestion had been made that the link between BDNF and psychopathology ought to be re-evaluated [24]
Summary
Increasing attention has been devoted to the possibility that growth factors, such as brain derived neurotrophic factor (BDNF), through actions on neurogenesis and neuroplasticity, contribute to the evolution of depressive disorders [1] In this regard, BDNF, which normally provides trophic support for neurons, is reduced in response to stressors [2], and serum levels of this trophic factor were lower in depressed patients than in controls [3,4]. Positive treatment responses elicited by SSRI treatment were accompanied by increased serum BDNF levels [6,7] These studies indicate that BDNF might be a biomarker for depression, they don’t speak to the possibility that peripheral BDNF might contribute to this disorder. This said, in animals, systemic BDNF treatment reduced signs of anxiety in several behavioral tests coincident with increased hippocampal neurogenesis, suggesting a causal role for peripheral BDNF in promoting behavioral changes [8]
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