Negative Processing Bias Research Articles

Abstract # 3184 Low grade inflammation induces negative bias in categorization of emotional information

Negative processing biases towards valenced information are a hallmark of depression. We set out to test whether peripheral inflammation can induce such negative interpretation biases. Forty healthy adult men received Salmonella Typhi vaccination and placebo injections on two separate days, using a double-blind crossover design. Blood samples were taken at baseline, 5.5h and 8h post-injection. The participants completed the P1vital® Oxford Emotional Test Battery, which included a Facial Expression Recognition Task (in which a range of intensities of six emotional facial expressions are classified) and Emotional Categorisation and Recall tasks (in which personality descriptors are categorized as positive or negative, and also later recalled). Vaccination increased Interleukin-6 from 1.18 to a peak of 5.21pg/mL at 5.5h post injection (p

Depression risk and electrocortical reactivity during self-referential emotional processing in 8 to 14 year-old girls.

Cognitive vulnerabilities, such as a negative self-referential processing bias, have been theorized to play a causal role in the development of depression. Indeed, depression is associated with the endorsement and recall of more negative and fewer positive emotional words (i.e., recall biases) in the self-referential encoding task (SRET). In addition, currently depressed adults and adolescents, compared to healthy controls, show an enhanced late positive potential (LPP), an event-related potential (ERP) component that reflects sustained attentional engagement, during the processing of negative relative to positive words in the SRET. However, it is unclear whether these behavioral and neural measures in the SRET are indicators of risk for depression, or are concomitants of the disorder. The present study included 121 8 to 14 year-old girls with no lifetime history of depression, and examined the association between maternal history of depression (i.e., risk) and both behavioral and ERP measures while viewing positive and negative adjectives during the SRET. Lifetime history of major depressive disorder and/or dysthymia in the biological mother was assessed via a semistructured diagnostic interview. Results indicated that participants with maternal history of depression, compared with those with no maternal history of depression, demonstrated an enhanced LPP to negative words. There were no group differences in the LPP to positive words. Maternal history of depression was also related to faster response time when rejecting negative words. Participant's current depression symptoms were associated with increased negative recall bias and decreased positive recall bias. The present study provides novel evidence that abnormal electrocortical reactivity to negative self-referential words indexes vulnerability for depression in 8 to 14 year-old girls. (PsycINFO Database Record

Deficits of unconscious emotional processing in patients with major depression: An ERP study

BackgroundMajor depressive disorder (MDD) is associated with behavioral and neurobiological evidences of negative bias in unconscious emotional processing. However, little is known about the time course of this deficit. The current study aimed to explore the unconscious processing of emotional facial expressions in MDD patients by means of event-related potentials (ERPs). MethodsThe ERP responses to subliminally presented happy/neutral/sad faces were recorded in 26 medication-free patients and 26 healthy controls in a backward masking task. Three ERP components were compared between patients and controls. ResultsDetection accuracy was at chance level for both groups, suggesting that the process was performed in the absence of conscious awareness of the emotional stimuli. Robust emotion×group interactions were observed in P1, N170 and P3. Compared with the neutral faces, 1) the patients showed larger P1 for sad and smaller P1 for happy faces; however, the controls showed a completely inverse P1 pattern; 2) the controls exhibited larger N170 in the happy but not in the sad trials, whereas patients had comparable larger N170 amplitudes in sad and happy trials; 3) although both groups exhibited larger P3 for emotional faces, the patients showed a priority for sad trials while the controls showed a priority for happy trials. ConclusionOur data suggested that negative processing bias exists on the unconscious level in individuals with MDD. The ERP measures indicated that the unconscious emotional processing in MDD patients has a time course of three-stage deflection.

Impact of 5-HTTLPR on SSRI serotonin transporter blockade during emotion regulation: A preliminary fMRI study

BackgroundThe short (‘S’) allele of the serotonin transporter (5-HTT)-linked polymorphic region (5-HTTLPR) is associated with increased negative emotion processing bias, and this polymorphism moderates acute effects of selective serotonin reuptake inhibitor (SSRI) treatment. In this preliminary study, we explore the moderating effect of 5-HTTLPR on the impact of the SSRI, escitalopram during emotion regulation of negative emotional stimuli. MethodThirty-six healthy Caucasian, female participants underwent two fMRI scanning sessions following single dose escitalopram and placebo administration separated by a seven-day washout period according to a double-blind, randomized, placebo-controlled crossover design. Functional connectivity analysis was employed with a left (L) amygdala seed and a right interior frontal gyrus (R IFG) target. ResultsChanges in functional connectivity with emotion regulation and treatment were linearly related to 5-HTTLPR ‘L’ allele load such that negative R IFG-L amygdala connectivity was increased with an increasing number of ‘L’ alleles. Therefore, escitalopram may facilitate the effects of reappraisal by enhancing negative functional connectivity, a finding that is greatest in participants homozygous for the ‘L’ allele and least in those homozygous for the ‘S’ allele. LimitationsSub-samples of the homozygote ‘S/S’ and ‘L/L’ 5-HTTLPR groupings were small. However, the within-subjects nature of the experiment and observing changes at the individual subject level increases our confidence in the findings of the present study. ConclusionsThe present study elucidates a potential neural mechanism by which antidepressant treatment produces differential treatment outcomes dependent on the 5-HTTLPR polymorphism, providing new and important leads for models of antidepressant action.

Transgenerational effects of maternal depression on affect recognition in children

BackgroundThe association between maternal depression and adverse emotional and behavioral outcomes in children is well established. One associated factor might be altered affect recognition which may be transmitted transgenerationally. Individuals with history of depression show biased recognition of sadness. Our aim was to investigate parallels in maternal and children's affect recognition with remitted depressed mothers. Methods60 Mother–child dyads completed an affect recognition morphing task. We examined two groups of remitted depressed mothers, with and without history of physical or sexual abuse, and a group of healthy mothers without history of physical or sexual abuse. Children were between 5 and 12 years old. ResultsAcross groups, mothers identified happy faces fastest. Mothers with remitted depression showed a higher accuracy and response bias for sadness. We found corresponding results in their children. Maternal and children's bias and accuracy for sadness were positively correlated. Effects of remitted depression were found independent of maternal history of physical or sexual abuse. LimitationsOur sample size was relatively small and further longitudinal research is needed to investigate how maternal and children's affect recognition are associated with behavioral and emotional outcomes in the long term. ConclusionsOur data suggest a negative processing bias in mothers with remitted depression which might represent both the perpetuation of and vulnerability to depression. Children of remitted depressed mothers appear to be exposed to this processing bias outside acute depressive episodes. This may promote the development of a corresponding processing bias in the children and could make children of depressed mothers more vulnerable to depressive disorders themselves.

Facilitation of emotion regulation with a single dose of escitalopram: A randomized fMRI study

Acute antidepressant administration modulates neural activity consistent with decreases in negative emotion processing bias. However, studies are yet to examine whether treatment facilitates neural activity during reappraisal, an adaptive emotion regulation strategy associated with behavioral treatment response. Here we examine the impact of acute administration on reappraisal of negative stimuli using pharmaco-fMRI. Thirty-six healthy female participants completed two sessions of fMRI scanning, separated by a one-week washout period. A single dose of the selective serotonin reuptake inhibitor, escitalopram (20mg) was administered to participants using a double-blind, randomized, placebo-controlled crossover design. When participants were administered escitalopram (relative to a placebo) and asked to reappraise negative emotional stimuli, left amygdala activation was decreased and right inferior frontal gyrus (R IFG) activation was increased. Also observed was a greater negative left amygdala-R IFG functional connectivity when participants were administered escitalopram relative to placebo, and this change in connectivity was associated with reductions in subjective ratings of valence and arousal of negative stimuli. Further analysis revealed connectivity modulation across multiple frontal regions. Results suggest that the acute effect of a commonly prescribed antidepressant may include facilitating the regulation of negative emotional stimuli, providing new important leads for models of antidepressant action.

Self-referential processing in depressed adolescents: A high-density event-related potential study.

Despite the alarming increase in the prevalence of depression during adolescence, particularly among female adolescents, the pathophysiology of depression in adolescents remains largely unknown. Event-related potentials (ERPs) provide an ideal approach to investigate cognitive-affective processes associated with depression in adolescents, especially in the context of negative self-referential processing biases. In this study, healthy (n = 30) and depressed (n = 22) female adolescents completed a self-referential encoding task while ERP data were recorded. To examine cognitive-affective processes associated with self-referential processing, P1, P2, and late positive potential (LPP) responses to negative and positive words were investigated, and intracortical sources of scalp effects were probed using low-resolution electromagnetic tomography (LORETA). Additionally, we tested whether key cognitive processes (e.g., maladaptive self-view, self-criticism) previously implicated in depression related to ERP components. Relative to healthy female subjects, depressed females endorsed more negative and fewer positive words, and free recalled and recognized fewer positive words. With respect to ERPs, compared with healthy female adolescents, depressed adolescents exhibited greater P1 amplitudes following negative words, which was associated with a more maladaptive self-view and self-criticism. In both early and late LPP responses, depressed females showed greater activity following negative versus positive words, whereas healthy females demonstrated the opposite pattern. For both P1 and LPP, LORETA revealed reduced inferior frontal gyrus activity in response to negative words in depressed versus healthy female adolescents. Collectively, these findings suggest that the P1 and LPP reflect biased self-referential processing in female adolescents with depression. Potential treatment implications are discussed. (PsycINFO Database Record

Individual Differences in Response to Prediction Bias Training

Depressed and dysphoric individuals predict negative outcomes more often than healthy individuals, and more frequently than positive outcomes. However, it is unclear if there is a causal relationship between negative emotional processing biases and depressive symptoms. We examined whether prediction-targeted neurocognitive training changed symptoms, behavior, and physiological reactivity to positive or negative feedback in euthymic and dysphoric undergraduates. Participants were randomized to a positive training intervention or neutral training. Among participants who received the positive training, pupillary reactivity to negative feedback predicted decreased symptoms and decreased after each session. Neither effect was present in the neutral training group. Both groups were more likely than controls to predict positive outcomes after training. Data suggested that change in a physiological mechanism indexing emotional reactivity and change in depressive symptoms during a targeted intervention may be related, and that it is possible, using psychophysiology, to predict which individuals will respond to neurocognitive intervention.

Stability of self-referent encoding task performance and associations with change in depressive symptoms from early to middle childhood

Depressed individuals exhibit memory biases on the self-referent encoding task (SRET), such that those with depression exhibit poorer recall of positive, and enhanced recall of negative, trait adjectives (referred to as positive and negative processing biases). However, it is unclear when SRET biases emerge, whether they are stable, and if biases predict, or are predicted by, depressive symptoms. To address this, a community sample of 434 children completed the SRET and a depressive symptoms measure at ages 6 and 9. Negative and positive processing exhibited low, but significant, stability. At ages 6 and 9, depressive symptoms correlated with higher negative, and lower positive, SRET processing. Importantly, lower positive processing at age 6 predicted increased symptoms at age 9. However, negative processing at age 6 did not predict depressive symptoms at age 9, and depressive symptoms at age 6 did not predict SRET processing scores at age 9. This suggests that less positive processing may reflect vulnerability for future depressive symptoms.

The impact of 5-HTTLPR on acute serotonin transporter blockade by escitalopram on emotion processing: preliminary findings from a randomised, crossover fMRI study.

Benefit from antidepressant treatment such as selective serotonin reuptake inhibitors (SSRIs) may depend on individual differences in acute effects on neural emotion processing. The short ('S') allele of the serotonin transporter (5-HTT)-linked polymorphic region (5-HTTLPR) is associated with both negative emotion processing biases and poorer treatment outcomes. Therefore, the aim of the present study was to explore the effects of 5-HTTLPR on the impact of the SSRI escitalopram during processing of positive and negative emotional images, as well as neutral stimuli. The study employed a double-blind, randomised, placebo-controlled crossover design on 36 healthy Caucasian female participants who underwent functional magnetic resonance imaging (fMRI) scanning following placebo or escitalopram treatment, separated by a 7-day washout period. Changes in the left amygdala signal with escitalopram treatment during processing of emotional stimuli were linearly related to the 5-HTTLPR 'S' allele load such that the signal to positive stimuli decreased and the signal to negative stimuli increased with an increasing number of low-expressing 'S' alleles. While 5-HTTLPR subgroups were small in size, individual subject changes with treatment and task condition increase confidence in the findings. While preliminary, our findings comprise the first pharmacogenetic study demonstrating an effect of the 5-HTTLPR 'S' allele load on escitalopram-induced changes in amygdala activity during emotional processing, consistent with a 5-HTT expression dosage model. The present findings have implications for the impact of this polymorphism on antidepressant efficacy in patients with mood and anxiety disorders.

EPA-1001 - Molecular Underpinnings of Cognitive and Emotion Processing in Mood Disorders

Mood disorders have been frequently associated with limbic hyper-responsiveness to emotionally negative stimuli as measured with functional magnetic resonance imaging (fMRI). Such aberrations of limbic, and particularly amygdala activity during emotion processing appear to be associated with negative cognitive processing biases implicated in the onset and maintenance of depression. In a series of studies, the authors investigated molecular underpinnings of pathological amygdala function using different fMRI paradigms designed to target automatic and controlled stages of emotion processing. Strong effects of selected candidate genotypes and amygdala responsiveness as well as amygdalaprefrontal coupling were observed across independent samples of depressed patients and healthy control subjects, supporting the notion of genetically influenced brain activation patterns associated with mood disorders. The frequently investigated 5-HTTLPR polymorphism was linked to amygdala hyper-responsiveness to negative but not positive facial expressions in paradigms assessing automatic amygdala responsiveness by means of subliminally presented stimuli. In later, controlled stages of emotion processing, genetic variations in COMT, MAO-A, Neuropeptides, and pro-inflammatory cytokines were associated with amygdala activity and amygdala-prefrontal coupling, pointing to dysfunctions in emotion regulation circuitries. In forthcoming studies, gene x environment interaction and epigenetic markers such as DNA methylation will inform about the degree of genetic and environmental influence on brain activation patterns in mood disorders.

Changes in the neural correlates of implicit emotional face processing during antidepressant treatment in major depressive disorder

An emerging hypothesis regarding the mechanisms underlying antidepressant pharmacotherapy suggests that these agents benefit depressed patients by reversing negative emotional processing biases (Harmer, 2008). Neuropsychological indices and functional neuroimaging measures of the amygdala response show that antidepressant drugs shift implicit and explicit processing biases away from the negative valence and toward the positive valence. However, few studies have explored such biases in regions extensively connected with the amygdala, such as the pregenual anterior cingulate cortex (pgACC) area, where pre-treatment activity consistently has predicted clinical outcome during antidepressant treatment. We used functional magnetic resonance imaging (fMRI) to investigate changes in haemodynamic response patterns to positive vs. negative stimuli in patients with major depressive disorder (MDD) under antidepressant treatment. Participants with MDD (n = 10) underwent fMRI before and after 8 wk sertraline treatment; healthy controls (n = 10) were imaged across an equivalent interval. A backward masking task was used to elicit non-conscious neural responses to sad, happy and neutral face expressions. Haemodynamic responses to emotional face stimuli were compared between conditions and groups in the pgACC. The response to masked-sad vs. masked-happy faces (SN-HN) in pgACC in the depressed subjects was higher in the pre-treatment condition than in the post-treatment condition and this difference was significantly greater than the corresponding change across time in the controls. The treatment-associated difference was attributable to an attenuated response to sad faces and an enhanced response to happy faces. Pre-treatment pgACC responses to SN-HN correlated positively with clinical improvement during treatment. The pgACC participates with the amygdala in processing the salience of emotional stimuli. Treatment-associated functional changes in this limbic network may influence the non-conscious processing of such stimuli by reversing the negative processing bias extant in MDD.

Neuronal Coding of Implicit Emotion Categories in the Subcallosal Cortex in Patients with Depression

The subcallosal cingulate and adjacent ventromedial prefrontal cortex (collectively referred to here as the subcallosal cortex or SCC) have been identified as key brain areas in emotional processing. The SCC's role in affective valuation as well as severe mood and motivational disturbances, such as major depression, has been largely inferred from measures of neuronal population activity using functional neuroimaging. On the basis of imaging studies, it is unclear whether the SCC predominantly processes 1) negatively valenced affective content, 2) affective arousal, or 3) category-specific affective information. To clarify these putative functional roles of the SCC, we measured single neuron activity in the SCC of 15 human subjects undergoing deep brain stimulation for depression while they viewed emotionally evocative images grouped into categories that varied in emotional valence (pleasantness) and arousal. We found that the majority of responsive neurons were modulated by specific emotion categories, rather than by valence or arousal alone. Moreover, although these emotion-category-specific neurons responded to both positive and negative emotion categories, a significant majority were selective for negatively valenced emotional content. These findings reveal that single SCC neuron activity reflects the automatic valuational processing and implicit emotion categorization of visual stimuli. Furthermore, because of the predominance of neuronal signals in SCC conveying negative affective valuations and the increased activity in this region among depressed people, the effectiveness of depression therapies that alter SCC neuronal activity may relate to the down-regulation of a previously negative emotional processing bias.

Context insensitivity during positive and negative emotional expectancy in depression assessed with functional magnetic resonance imaging

Patients with depression show an enhanced preoccupation with negative expectations and are often unable to look forward to positive events. Here we studied anticipatory emotional processes in unmedicated depressed patients using functional magnetic resonance imaging. Consistent with a negative processing bias, we hypothesized enhanced responses to negative and attenuated responses to positive expectancy cues in brain areas associated with emotional expectancy. Participants comprised 19 drug-free depressed patients and 19 matched healthy control subjects who viewed affective photographs. Pictures were preceded by an expectancy cue which signaled the emotional valence of the upcoming picture in half of the trials. Depressed patients showed attenuated blood-oxygen-level-dependent responses in the left lateral prefrontal cortex (inferior frontal gyrus, Brodmann area 44) during positive expectancy and—contrary to our hypothesis—in the right lateral orbitofrontal cortex (middle frontal gyrus, Brodmann area 47) during negative expectancy. This attenuation was specific for the anticipation (as opposed to the perception) of emotional pictures and correlated with a clinical measure of depressive symptoms. The observed attenuation suggests emotion-context insensitivity rather than a negative processing bias during anticipatory emotional processes in depression. This hyporeactivity may contribute to clinical features like anergia, apathy, and loss of motivation in the context of both positive and negative incentives.

1269 – Reduced fractional anisotropy in the uncinate fasciculus in patients with major depression carrying the met-allele of the Val66Met brain-derived neurotrophic factor genotype

Experimental studies support a neurotrophic hypothesis of major depressive disorder (MDD). The aim of this study was to determine the effect of Val66Met brain derived neurotrophic factor (BDNF) polymorphism on the white matter fibre tracts connecting hippocampus and amygdala with the prefrontal lobe in a sample of patients with MDD and healthy controls. Thirty seven patients with MDD and 42 healthy volunteers were recruited. Diffusion tensor imaging (DTI) data with 61 diffusion directions were obtained with MRI 3 Tesla scanner. Deterministic tractography was applied with ExploreDTI and Val66Met BDNF SNP (rs6265) was genotyped. Fibre tracts connecting the hippocampus and amygdala with the prefrontal lobe, namely uncinate fasciculus, fornix and cingulum were analysed. A significant interaction was found in the uncinate fasciculus (UF) between BDNF alleles and diagnosis. Patients carrying the BDNF met-allele had smaller fractional anisotropy (FA) in the UF compared to those patients homozygous for valallele and compared to healthy subjects carrying the met-allele. A significant 3-way interaction was detected between region of the cingulum (dorsal, rostral and parahippocampal regions), brain hemisphere and BDNF genotype. Larger FA was detectable in the left rostral cingulum for met-allele carriers when compared to val/val alelle carriers. We provide evidence for the importance of the neurotrophic involvement in limbic and prefrontal connections. The met-allele of the BDNF polymorphism seems to render subjects more vulnerable for dysfunctions associated with the UF, a tract known to be related to negative emotional-cognitive processing bias, declarative memory problems, and autonoetic self awareness.

Never-depressed females with a family history of depression demonstrate affective bias

According to cognitive theories of depression, individuals susceptible to depression attend selectively to negative information. The purpose of the study was to examine if such an affective processing bias is present in never-depressed individuals with a family history of major depressive disorder (MDD). Formerly depressed female patients having at least one first-degree relative with a history of MDD (n=23), their never-depressed female siblings (n=21) and never-depressed female controls (n=21) performed a conventional and an emotional Stroop task using negative, positive and neutral words. A significant effect was found of group on negative processing bias; post hoc comparisons indicated that never-depressed siblings showed a larger negative processing bias than never-depressed controls. No significant differences were observed in positive bias or conventional interference between the three groups. Our findings suggest that never-depressed females with a family history of depression, like depressed patients, have more difficulties to inhibit negative material and to direct their attention towards task-specific material. This adds to the existing evidence that affective processing bias is a trait characteristic that contributes to the onset of depression and that could be a useful endophenotype for MDD.

Increased Amygdala Responses to Sad But Not Fearful Faces in Major Depression: Relation to Mood State and Pharmacological Treatment

Increased amygdala response to negative emotions seen in functional MRI (fMRI) has been proposed as a biomarker for negative emotion processing bias underlying depressive symptoms and vulnerability to depressive relapse that are normalized by antidepressant drug treatment. The purpose of this study was to determine whether abnormal amygdala responses to face emotions in depression are related to specific emotions or change in response to antidepressant treatment and whether they are present as a stable trait in medication-free patients in remission. Sixty-two medication-free unipolar depressed patients (38 were currently depressed, and 24 were in remission) and 54 healthy comparison subjects underwent an indirect face-emotion processing task during fMRI. Thirty-two currently depressed patients were treated with the antidepressant citalopram for 8 weeks. Adherence to treatment was evaluated by measuring citalopram plasma concentrations. Patients with current depression had increased bilateral amygdala responses specific to sad faces relative to healthy comparison subjects and nonmedicated patients in stable remission. Treatment with citalopram abolished the abnormal amygdala responses to sad faces in currently depressed patients but did not alter responses to fearful faces. Aberrant amygdala activation in response to sad facial emotions is specific to the depressed state and is a potential biomarker for a negative affective bias during a depressive episode.

Childhood maltreatment is associated with an automatic negative emotion processing bias in the amygdala

Major depression has been repeatedly associated with amygdala hyper-responsiveness to negative (but not positive) facial expressions at early, automatic stages of emotion processing using subliminally presented stimuli. However, it is not clear whether this "limbic bias" is a correlate of depression or represents a vulnerability marker preceding the onset of the disease. Because childhood maltreatment is a potent risk factor for the development of major depression in later life, we explored whether childhood maltreatment is associated with amygdalar emotion processing bias in maltreated but healthy subjects. Amygdala responsiveness to subliminally presented sad and happy faces was measured by means of fMRI at 3 T in N = 150 healthy subjects carefully screened for psychiatric disorders. Childhood maltreatment was assessed by the 25-item childhood trauma questionnaire (CTQ). A strong association of CTQ-scores with amygdala responsiveness to sad, but not happy facial expressions emerged. This result was further qualified by an interaction of emotional valence and CTQ-scores and was not confounded by trait anxiety, current depression level, age, gender, intelligence, education level, and more recent stressful life-events. Childhood maltreatment is apparently associated with detectable changes in amygdala function during early stages of emotion processing which resemble findings described in major depression. Limbic hyper-responsiveness to negative facial cues could be a consequence of the experience of maltreatment during childhood increasing the risk of depression in later life. the present association of limbic bias and maltreatment was demonstrated in the absence of psychopathological abnormalities, thereby limiting strong conclusions.

Reduced fractional anisotropy in the uncinate fasciculus in patients with major depression carrying the met‐allele of the Val66Met brain‐derived neurotrophic factor genotype

Experimental studies support a neurotrophic hypothesis of major depressive disorder (MDD). The aim of this study was to determine the effect of Val66Met brain-derived neurotrophic factor (BDNF) polymorphism on the white matter fiber tracts connecting hippocampus and amygdala with the prefrontal lobe in a sample of patients with MDD and healthy controls. Thirty-seven patients with MDD and 42 healthy volunteers were recruited. Diffusion tensor imaging (DTI) data with 61 diffusion directions were obtained with MRI 3 Tesla scanner. Deterministic tractography was applied with ExploreDTI and Val66Met BDNF SNP (rs6265) was genotyped. Fiber tracts connecting the hippocampus and amygdala with the prefrontal lobe, namely uncinate fasciculus (UF), fornix, and cingulum were analyzed. A significant interaction was found in the UF between BDNF alleles and diagnosis. Patients carrying the BDNF met-allele had smaller fractional anisotropy (FA) in the UF compared to those patients homozygous for val-allele and compared to healthy subjects carrying the met-allele. A significant three-way interaction was detected between region of the cingulum (dorsal, rostral, and parahippocampal regions), brain hemisphere and BDNF genotype. Larger FA was detectable in the left rostral cingulum for met-allele carriers when compared to val/val alelle carriers. We provide evidence for the importance of the neurotrophic involvement in limbic and prefrontal connections. The met-allele of the BDNF polymorphism seems to render subjects more vulnerable for dysfunctions associated with the UF, a tract known to be related to negative emotional-cognitive processing bias, declarative memory problems, and autonoetic self awareness.

Evaluating the Mood State Dependence of Automatic Thoughts and Dysfunctional Attitudes in Remitted Versus Never-Depressed Individuals

The cognitive model of depression specifies the role of schema-driven negative processing biases in the onset and maintenance of depression. Research has shown that cognitive reactivity, or the ease with which negative thinking patterns are activated by mild changes in negative mood, is related to relapse and recurrence. The goal of this study was to examine cognitive reactivity following a mood prime in individuals vulnerable to depression. Formerly (n = 28) and never (n = 36) depressed individuals were assessed on two measures of negative cognition, the Automatic Thoughts Questionnaire (ATQ) and Dysfunctional Attitudes Scale (DAS), before and after participating in a sad or neutral mood induction procedure (MIP). The negative mood induction resulted in increased belief in negative automatic thoughts across groups; however, only the formerly depressed participants assigned to this condition demonstrated increased DAS scores. Importantly, individuals who completed the neutral mood induction did not exhibit increases in negative cognition, providing evidence against the possibility that the MIP itself may lead to increases in negative cognition. These findings are discussed in relation to understanding the role of negative cognition and vulnerability to depression.