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  • Addiction, Drugs
  • Information from Lay-Language Summaries is Embargoed Until the Conclusion of the Scientific Presentation

    013—Mood Disorders: Human Biomarkers, Treatment, and Post Mortem Studies

    Saturday, November 09, 2013, 1:00 pm - 3:15 pm

    13.08: Hyperresponsive amygdala in healthy 14-year-old adolescents with family history of depression

    Location: 30B

    *M. PILHATSCH, N. C. VETTER, T. H‹BNER, M. N. SMOLKA;
    Dpt. of Psychiatry and Psychotherapy, Technische Univ. Dresden, Dresden, Germany

    Abstract Body: Previous fMRI studies demonstrated altered activity of the amygdala in manifest depression, in juvenile offspring (diagnosed with anxiety disorder or ADHD) of parents with Major Depression as well as in vulnerable subjects with high neuroticism. We predicted to detect a hyperresponsive amygdala in 14 year old participants with positive family history of depression, in which no psychopathology has manifested so far, as compared with peers having no family history of psychiatric disorders. Within our sample of 164 adolescents 28 fulfilled criteria for positive family history of depression and 136 served as controls. Both groups were similar in terms of sex, IQ, pubertal status, depressive symptomatology and anxiety. During fMRI scanning they performed an emotional processing task in which visual stimuli were systematically modified in terms of emotional valence and attentional dimension.
    A full factorial ANOVA revealed a group-by-attention-by-valence (negative-neutral) interaction in both amygdalae in a whole brain analysis. No other brain region survived the statistical threshold (p < .001/ uncorr.; p ≤ .05 /FWEcorr.). Post-hoc analyzes revealed that negatively valenced distractors elicit a stronger BOLD response in both amygdalae of family-history-positive subjects compared to controls. Additionally, within the risk population amygdala activation was significantly greater during the processing of negative compared to neutral stimuli when attention was directed to a non-emotional primary task. This was not the case in the control population.
    Our results demonstrate that adolescents at high risk for major depressive disorder relative to that at low risk showed greater amygdala activation during implicit processing of negative stimuli. Secondly, our results suggest a neural correlate of an attentional capture effect of negative stimuli driven by family history of depression.
    These findings point to the early occurrence of a subtle emotional processing bias that is associated with negative cognitive distortions typically found in Major Depression.

    Lay Language Summary: Our brain imaging study indicates that family history of depression, i.e. major depression occurring in parents or grandparents, affects an individual’s development of brain regions related to emotional processing. An altered function of these regions might then increase the risk of developing a depression later in life.
    Research has shown that children whose parents suffer from major depression have a three-fold higher risk of being affected by depressive disorders during their lifetime. However, the mechanisms underlying this increased risk are still unknown.
    Previous neuroimaging studies have demonstrated that brain function in adults suffering from manifest depression as well as in adults considered as being at risk for depression is altered in the amygdala, a brain area which evaluates emotional, especially negative stimuli. Hyperreactivity of the amygdala has been linked to negatively biased emotional processing, typically observed in depressed patients, who tend to overemphasize negative aspects and keep them longer in mind. However, no study has elucidated so far, if similar perturbations of the amygdala can be found in healthy adolescents with family history of depression.
    To explore if family history of depression affects the neural functions underlying the processing of emotional pictures in burdened offspring we used data from a prospective, longitudinal community study with 164 healthy 14-year-old adolescents. 28 of them had at least one relative affected by depression. Adolescents with past or current psychiatric disorders were excluded and groups did not differ with regard to intelligence, psychopathology or experience of negative life-events.
    All adolescents performed a task in which pairs of negative, neutral and positive pictures were presented either as targets, to be matched or as distractors to be ignored during a matching task of abstract pictures. During the whole task, brain activation of participants was measured with functional magnetic resonance imaging (fMRI).
    Adolescents with family history of depression responded with higher activity in brain areas related to emotional processing, more precisely in the amygdala during processing of negative compared to neutral distracting pictures. Increased responses to negative pictures in this brain area have been found in people suffering from depression, and are therefore thought to be a risk factor for the development of depressive disorder.
    Our study may help to understand how the neural mechanisms that give rise to depression manifest across the lifespan. We need further research to characterize the interrelationships of vulnerability to depression and modes of reaction in challenging life events from a neuro-developmental perspective. Therefore our project will follow up the same adolescents at the ages of 16 and 18. Follow-up assessments could aim to understand how changes in brain function lead to the manifestation of depression, opening the field for the development and appropriate timing of specific targeted preventive strategies that account for individual risk profiles.