5-HTTLPR

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Christopher G. Beevers - One of the best experts on this subject based on the ideXlab platform.

  • Associations between serotonin transporter gene promoter region (5-HTTLPR) polymorphism and gaze bias for emotional information.
    Journal of abnormal psychology, 2011
    Co-Authors: Christopher G. Beevers, C. Nathan Marti, Han-joo Lee, Deborah L. Stote, Robert E. Ferrell, Ahmad R. Hariri, Michael J. Telch
    Abstract:

    The serotonin transporter promoter region polymorphism (5-HTTLPR) is associated with neural response to negative images in brain regions involved in the experience of emotion. However, the behavioral implications of this sensitivity have been studied far less extensively. The current study used eye-tracking methodology to examine how individuals genotyped for the 5-HTTLPR, including the single nucleotide polymorphism (SNP) rs25531, allocated attention during prolonged (30-s) exposure to face stimuli depicting positive and negative emotion. Short 5-HTTLPR allele carriers and carriers of the long allele with guanine at the sixth nucleotide (S/LG) displayed a stronger gaze bias (total fixation time, number of fixations, mean fixation length) for positive than for sad, threat, or neutral stimuli. In contrast, those homozygous for the long 5-HTTLPR allele with adenine at the sixth nucleotide (LA) viewed the emotion stimuli in an unbiased fashion. Time course analyses indicated no initial 5-HTTLPR group differences; however, S/LG 5-HTTLPR allele carriers were more likely than LA 5-HTTLPR homozygotes to direct gaze toward happy than toward sad stimuli over time. This bias toward positive stimuli during the later stages of information processing likely reflects a strategic effort to downregulate heightened reactivity to negative stimuli among 5-HTTLPR S/LG allele carriers.

  • Prefrontal Morphology, 5-HTTLPR Polymorphism, and Biased Attention for Emotional Stimuli
    Genes brain and behavior, 2009
    Co-Authors: Christopher G. Beevers, John E. Mcgeary, Jennifer Pacheco, Peter C. Clasen, David M. Schnyer
    Abstract:

    Biased attention for emotional stimuli has been associated with vulnerability to psychopathology. This study examines the neural substrates of biased attention. Twenty-three adult women completed high-resolution structural imaging followed by a standard behavioral measure of biased attention (i.e. spatial cueing task). Participants were also genotyped for the serotonin transporter-linked promoter region (5-HTTLPR) gene. Results indicated that lateral prefrontal cortex (lPFC) morphology was inversely associated with maintained attention for positive and negative stimuli, but only among short 5-HTTLPR allele carriers. No such associations were observed for the medial prefrontal cortex (mPFC) or the amygdala. Results from this study suggest that brain regions involved in cognitive control of emotion are also associated with attentional biases for emotion stimuli among short 5-HTTLPR allele carriers.

  • Association of the serotonin transporter gene promoter region (5-HTTLPR) polymorphism with biased attention for emotional stimuli.
    Journal of abnormal psychology, 2009
    Co-Authors: Christopher G. Beevers, Tony T. Wells, Alissa J. Ellis, John E. Mcgeary
    Abstract:

    A deletion polymorphism in the serotonin transporter-linked polymorphic region (5-HTTLPR) has been associated with vulnerability to affective disorders, yet the mechanism by which this gene confers vulnerability remains unclear. Two studies examined associations between the 5-HTTLPR polymorphism and attentional bias for emotional stimuli among nondepressed adults. Biased attention, attention engagement, and difficulty with attention disengagement were assessed with a spatial cuing task using emotional stimuli. Results from Study 1 (N = 38) indicated that short 5-HTTLPR allele carriers experienced greater difficulty disengaging their attention from sad and happy stimuli compared with long allele homozygotes. Study 2 participants (N = 144) were genotyped for the 5-HTTLPR polymorphism, including single nucleotide polymorphism rs25531 in the long allele of the 5-HTTLPR. Consistent with Study 1, individuals homozygous for the low-expressing 5-HTTLPR alleles (i.e., S and LG) experienced greater difficulty disengaging attention from sad, happy, and fear stimuli than high-expressing 5-HTTLPR homozygotes. Because this association exists in healthy adults, it may represent a susceptibility factor for affective disorders that becomes problematic during stressful life experiences.

Andrew Smolen - One of the best experts on this subject based on the ideXlab platform.

  • Dysfunctional attitudes and the serotonin transporter promoter polymorphism (5-HTTLPR).
    Behavior therapy, 2011
    Co-Authors: Mark A. Whisman, Daniel P. Johnson, Andrew Smolen
    Abstract:

    Dysfunctional attitudes may be one phenotype by which genes increase risk for depression. Building on research demonstrating associations between serotonin abnormalities and dysfunctional attitudes, we examined the covariation between dysfunctional attitudes and the serotonin transporter gene-linked polymorphic region (5-HTTLPR). In a sample of nondepressed young adults (N=131), people with one or two copies of the low-expressing alleles reported stronger endorsement of dysfunctional attitudes regarding performance evaluation than people who were homozygous for the high-expressing alleles; there was no association between the 5-HTTLPR polymorphism and dysfunctional attitudes regarding approval by others. These results add to the literature linking the 5-HTTLPR polymorphism and cognitive vulnerabilities for depression.

  • Behavioral inhibition and triallelic genotyping of the serotonin transporter promoter (5-HTTLPR) polymorphism
    Journal of Research in Personality, 2011
    Co-Authors: Mark A. Whisman, Emily D. Richardson, Andrew Smolen
    Abstract:

    Abstract To examine the genetic bases of the behavioral inhibition system (BIS) and the behavioral approach system (BAS), we evaluated the association between the BIS, the BAS, and a functional length polymorphism in the promoter of the serotonin transporter gene (5-HTTLPR) in an unscreened sample of undergraduates ( N  = 211); analyses were conducted using a two-variant (i.e., biallelic) genotyping and three-variant (i.e., triallelic) genotyping of the 5-HTTLPR polymorphism. People with one or two copies of the low-expressing alleles reported stronger endorsement of the BIS than people who were homozygous for the high-expressing alleles; this association was found for triallelic but not biallelic genotyping of the 5-HTTLPR polymorphism. There was no association between the 5-HTTLPR polymorphism and the BAS scales.

Johann Daniel Kruschwitz - One of the best experts on this subject based on the ideXlab platform.

  • 5 httlpr rs25531 polymorphism and neuroticism are linked by resting state functional connectivity of amygdala and fusiform gyrus
    Brain Structure & Function, 2015
    Co-Authors: Johann Daniel Kruschwitz, Deepthi P Varikuti, Jimmy Jensen, Leila Haddad, Oliver Grimm, Sebastian Mohnke, Martin Walter, Michael M. Plichta, Lydia Pohland
    Abstract:

    The s/s-genotype of the 5-HTTLPR polymorphism and the personality trait of neuroticism have both been associated with experiences of negative affect, anxiety and mood disorders, as well as an emotional processing bias towards negative facial emotions. On a neural level, this bias can be characterized by altered amygdala and fusiform gyrus (FFG) activity during perception of negative facial expressions. Using resting-state functional magnetic resonance imaging in a multi-center-sample of 178 healthy subjects of European descent, this study investigated the association of 5-HTTLPR (short s- and long l-allele) including the genotype of the single nucleotide polymorphism (SNP) rs25531 (A/G) within this region polymorphism, and trait neuroticism on resting-state functional connectivity (rs-FC) between amygdala and the FFG. Moreover, we aimed to identify additional brain regions with associations of 5-HTTLPR/rs25531 (combined according to its expression; low: s/s; high: lA/lA; intermediate: s/lA, s/lG, lG/lG, lA/lG) and trait neuroticism to amygdala rs-FC. Separate analyses for 5-HTTLPR/rs25531 and neuroticism (controlling for age, gender, handedness, and research site) revealed that s/s-homozygotes and individuals high in neuroticism obtained altered amygdala rs-FC in the right occipital face area, which is considered to be a “core component” of the face processing system. Importantly, effects of neuroticism were replicated across three independent research sites. Additionally, associations of 5-HTTLPR/rs25531 genotype and amygdala rs-FC were observed in the anterior and posterior cingulate cortex, whereas neuroticism was not related to rs-FC in these areas. The presented data implies that 5-HTTLPR/rs25531 variants and neuroticism are linked by resting state functional connectivity of amygdala and fusiform gyrus and suggests that variants of 5-HTTLPR/rs25531 genotype and different levels of neuroticism may partly account for altered processing of negative facial emotions.

  • 5-HTTLPR/rs25531 polymorphism and neuroticism are linked by resting state functional connectivity of amygdala and fusiform gyrus
    Brain Structure & Function, 2014
    Co-Authors: Johann Daniel Kruschwitz, Deepthi P Varikuti, Jimmy Jensen, Leila Haddad, Oliver Grimm, Sebastian Mohnke, Lydia Pohland, Martin Walter, Michael M. Plichta, Bjorn H Schott
    Abstract:

    The s/s-genotype of the 5-HTTLPR polymorphism and the personality trait of neuroticism have both been associated with experiences of negative affect, anxiety and mood disorders, as well as an emotional processing bias towards negative facial emotions. On a neural level, this bias can be characterized by altered amygdala and fusiform gyrus (FFG) activity during perception of negative facial expressions. Using resting-state functional magnetic resonance imaging in a multi-center-sample of 178 healthy subjects of European descent, this study investigated the association of 5-HTTLPR (short s- and long l-allele) including the genotype of the single nucleotide polymorphism (SNP) rs25531 (A/G) within this region polymorphism, and trait neuroticism on resting-state functional connectivity (rs-FC) between amygdala and the FFG. Moreover, we aimed to identify additional brain regions with associations of 5-HTTLPR/rs25531 (combined according to its expression; low: s/s; high: lA/lA; intermediate: s/lA, s/lG, lG/lG, lA/lG) and trait neuroticism to amygdala rs-FC. Separate analyses for 5-HTTLPR/rs25531 and neuroticism (controlling for age, gender, handedness, and research site) revealed that s/s-homozygotes and individuals high in neuroticism obtained altered amygdala rs-FC in the right occipital face area, which is considered to be a “core component” of the face processing system. Importantly, effects of neuroticism were replicated across three independent research sites. Additionally, associations of 5-HTTLPR/rs25531 genotype and amygdala rs-FC were observed in the anterior and posterior cingulate cortex, whereas neuroticism was not related to rs-FC in these areas. The presented data implies that 5-HTTLPR/rs25531 variants and neuroticism are linked by resting state functional connectivity of amygdala and fusiform gyrus and suggests that variants of 5-HTTLPR/rs25531 genotype and different levels of neuroticism may partly account for altered processing of negative facial emotions.

John E. Mcgeary - One of the best experts on this subject based on the ideXlab platform.

  • Prefrontal Morphology, 5-HTTLPR Polymorphism, and Biased Attention for Emotional Stimuli
    Genes brain and behavior, 2009
    Co-Authors: Christopher G. Beevers, John E. Mcgeary, Jennifer Pacheco, Peter C. Clasen, David M. Schnyer
    Abstract:

    Biased attention for emotional stimuli has been associated with vulnerability to psychopathology. This study examines the neural substrates of biased attention. Twenty-three adult women completed high-resolution structural imaging followed by a standard behavioral measure of biased attention (i.e. spatial cueing task). Participants were also genotyped for the serotonin transporter-linked promoter region (5-HTTLPR) gene. Results indicated that lateral prefrontal cortex (lPFC) morphology was inversely associated with maintained attention for positive and negative stimuli, but only among short 5-HTTLPR allele carriers. No such associations were observed for the medial prefrontal cortex (mPFC) or the amygdala. Results from this study suggest that brain regions involved in cognitive control of emotion are also associated with attentional biases for emotion stimuli among short 5-HTTLPR allele carriers.

  • Association of the serotonin transporter gene promoter region (5-HTTLPR) polymorphism with biased attention for emotional stimuli.
    Journal of abnormal psychology, 2009
    Co-Authors: Christopher G. Beevers, Tony T. Wells, Alissa J. Ellis, John E. Mcgeary
    Abstract:

    A deletion polymorphism in the serotonin transporter-linked polymorphic region (5-HTTLPR) has been associated with vulnerability to affective disorders, yet the mechanism by which this gene confers vulnerability remains unclear. Two studies examined associations between the 5-HTTLPR polymorphism and attentional bias for emotional stimuli among nondepressed adults. Biased attention, attention engagement, and difficulty with attention disengagement were assessed with a spatial cuing task using emotional stimuli. Results from Study 1 (N = 38) indicated that short 5-HTTLPR allele carriers experienced greater difficulty disengaging their attention from sad and happy stimuli compared with long allele homozygotes. Study 2 participants (N = 144) were genotyped for the 5-HTTLPR polymorphism, including single nucleotide polymorphism rs25531 in the long allele of the 5-HTTLPR. Consistent with Study 1, individuals homozygous for the low-expressing 5-HTTLPR alleles (i.e., S and LG) experienced greater difficulty disengaging attention from sad, happy, and fear stimuli than high-expressing 5-HTTLPR homozygotes. Because this association exists in healthy adults, it may represent a susceptibility factor for affective disorders that becomes problematic during stressful life experiences.

Mark A. Whisman - One of the best experts on this subject based on the ideXlab platform.

  • Dysfunctional attitudes and the serotonin transporter promoter polymorphism (5-HTTLPR).
    Behavior therapy, 2011
    Co-Authors: Mark A. Whisman, Daniel P. Johnson, Andrew Smolen
    Abstract:

    Dysfunctional attitudes may be one phenotype by which genes increase risk for depression. Building on research demonstrating associations between serotonin abnormalities and dysfunctional attitudes, we examined the covariation between dysfunctional attitudes and the serotonin transporter gene-linked polymorphic region (5-HTTLPR). In a sample of nondepressed young adults (N=131), people with one or two copies of the low-expressing alleles reported stronger endorsement of dysfunctional attitudes regarding performance evaluation than people who were homozygous for the high-expressing alleles; there was no association between the 5-HTTLPR polymorphism and dysfunctional attitudes regarding approval by others. These results add to the literature linking the 5-HTTLPR polymorphism and cognitive vulnerabilities for depression.

  • Behavioral inhibition and triallelic genotyping of the serotonin transporter promoter (5-HTTLPR) polymorphism
    Journal of Research in Personality, 2011
    Co-Authors: Mark A. Whisman, Emily D. Richardson, Andrew Smolen
    Abstract:

    Abstract To examine the genetic bases of the behavioral inhibition system (BIS) and the behavioral approach system (BAS), we evaluated the association between the BIS, the BAS, and a functional length polymorphism in the promoter of the serotonin transporter gene (5-HTTLPR) in an unscreened sample of undergraduates ( N  = 211); analyses were conducted using a two-variant (i.e., biallelic) genotyping and three-variant (i.e., triallelic) genotyping of the 5-HTTLPR polymorphism. People with one or two copies of the low-expressing alleles reported stronger endorsement of the BIS than people who were homozygous for the high-expressing alleles; this association was found for triallelic but not biallelic genotyping of the 5-HTTLPR polymorphism. There was no association between the 5-HTTLPR polymorphism and the BAS scales.