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Genes involved in neuroplasticity and stressful life events act on the short‐term response to antidepressant treatment: a complex interplay between genetics and environment
Author(s) -
Mandelli Laura,
Emiliani Roberta,
Porcelli Stefano,
Fabbri Chiara,
Albani Diego,
Serretti Alessandro
Publication year - 2014
Publication title -
human psychopharmacology: clinical and experimental
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.461
H-Index - 78
eISSN - 1099-1077
pISSN - 0885-6222
DOI - 10.1002/hup.2411
Subject(s) - antidepressant , mood , single nucleotide polymorphism , stressor , neuroplasticity , anxiety , psychology , mood disorders , medicine , gene , psychiatry , genetics , genotype , biology
Objective During the last few years, an increasing number of studies have focused on the association between neuroplasticity and affective disorders. The aim of the study is to evaluate the interactive effect of stressful life events (SLEs) and genes involved in neuroplasticity (BDNF and ST8SIA) on the short‐term response to antidepressant treatment. Methods A total of 114 patients affected by mood or anxiety disorders under antidepressant treatment were enrolled in the study. We evaluated the interactive effects of three BDNF single‐nucleotide polymorphisms (SNPs) and five ST8SIA SNPs and SLEs at different time points (childhood SLEs, SLEs at illness onset, and SLEs reported over the last preceding treatment) over 1‐month of antidepressant treatment. Results Carriers of some genetic variants in both BDNF and ST8SIA had a slower response to antidepressants if non‐exposed to the onset SLEs, whereas they had a similar trend compared with the carriers of the opposite variant if exposed (allelic analysis: BDNF p = 0.00003, p = 0.00609; ST8SIA p = 0.04, p = 0.033). The BDNF haplotype analysis confirmed this trend ( p = 0.00016). Conclusions Though our results are limited by the small sample size, variants in BDNF and ST8SIA may slow down the early response to antidepressants in subjects non‐exposed to stressors at the illness onset, with a remarkable gene–environment interaction. Copyright © 2014 John Wiley & Sons, Ltd.