Here using mediated moderation analysis, we show that electrophysiological manifestations of resting state networks in the alpha frequency band mediate the effect of 5-HTTLPR by stress interaction on depression/anxiety symptoms in a nonclinical sample.
The aim of this study was to investigate the relationship between genotypic variation in six candidate serotonergic genes (ADCY9, HTR1B, GNB3, HTR2A, TPH2, SLC6A4) and depressive and anxiety symptom severity trajectories as well as remission following escitalopram treatment.
To ascertain whether genetic variations in the serotonin transporter gene (5-HTTLPR 44-bp insertion/deletion polymorphism) influence an increase in depressive and anxiety symptoms in children and adolescents exposed to high levels of violence.
Unmedicated, young adults with low current depression and anxiety symptoms (N=106) were genotyped for the 5-HTTLPR, including the single nucleotide polymorphism (SNP) rs25531 in the long allele of the 5-HTTLPR.
Since serotonin-synthesizing neurons are known to be lost in the AD cortex, this study suggests that the preservation of 5-HTT may exacerbate serotonergic deficits and underlie anxiety symptoms in AD.