Abstract
The PCLO rs2522833 candidate polymorphism for depression has been associated to monoaminergic neurotransmission. In healthy and currently depressed individuals, the polymorphism has been found to affect activation of brain areas during memory processing, but no direct association of PCLO with memory bias was found. We hypothesized that the absence of this association might have been obscured by current depressive symptoms or genetically driven individual differences in reactivity to stressful events. Experiencing stressful childhood events fosters dysfunctional assumptions that are related to cognitive biases, and may modulate the predisposition for depression via epigenetic effects. The association between PCLO and memory bias, as well as interaction between PCLO and childhood events was studied in patients remitted from depression (N = 299), as well as a sample of healthy individuals (N = 157). The participants performed an emotional verbal memory task after a sad mood induction. Childhood trauma and adversity were measured with a questionnaire. The Genotype main effect, and Genotype by Childhood Events interaction were analyzed for memory bias in both samples. PCLO risk allele carrying remitted depressed patients did not show more negatively biased memory than non-risk allele carriers, not even patients with stressful childhood events. A similar pattern of results was found in healthy individuals. Memory bias may not be strongly associated with the PCLO rs2522833 polymorphism. We did not find any support for the PCLO-childhood events interaction, but the power of our study was insufficient to exclude this possibility.
Highlights
Depression results in a high disease burden as well as increased mortality risk due to important impairments in social, emotional and physical functioning
The C ‘risk’ allele is more frequent in depressed individuals than in healthy individuals and has been associated with heritable personality traits that predispose to depression in healthy individuals, such as ‘harm avoidance’ [4], as well as with changes in HPA responsiveness after treatment [9]
The study was approved by the Dutch Central Committee on Research involving Human Subjects (CCMO) and we complied with the Code of Ethics of the World Medical Association (Declaration of Helsinki) in the treatment of our participants
Summary
Depression results in a high disease burden as well as increased mortality risk due to important impairments in social, emotional and physical functioning. The SNP rs2522833 in the piccolo (PCLO) gene has been associated with current depression [2,3,4,5]. The PCLO gene encodes a presynaptic cytomatrix protein called piccolo. Monoaminergic modulation of the hypothalamic pituitary adrenal system (involved in stress responses) may be a route through which PCLO affects depression vulnerability [4,8,9]. The C ‘risk’ allele is more frequent in depressed individuals than in healthy individuals and has been associated with heritable personality traits that predispose to depression in healthy individuals, such as ‘harm avoidance’ [4], as well as with changes in HPA responsiveness after treatment [9]. Other studies were not able to replicate the association with clinical depression [7], or did not find an association with sub-clinical levels of depression [3]
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