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      Reduced Hippocampal and Amygdala Volumes as Mechanisms of Stress Sensitization to Depression following Childhood Violence Exposure

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          Abstract

          OBJECTIVE

          Stressful life events are more likely to trigger depression among individuals exposed to childhood adversity. However, the mechanisms underlying this stress sensitization remain largely unknown. Any such mechanism must be altered by childhood adversity and interact with recent stressful life events, magnifying their association with depression. This study investigated whether reduced hippocampal and amygdala volumes are mechanisms of stress sensitization following childhood violence exposure.

          METHODS

          A sample of 149 youth (aged 8-17 years), with (N=76) and without (N=73) exposure to physical abuse, sexual abuse, or domestic violence participated. Participants completed a structural MRI scan and were assessed for symptoms of depression. Approximately two years later, stressful life events were assessed along with depression symptoms in 120 participants (57 violence-exposed).

          RESULTS

          Childhood violence exposure was associated with smaller hippocampal and amygdala volumes. Stressful life events occurring during the follow-up period predicted worsening depression over time, and this association was magnified among those with smaller hippocampal and amygdala volumes. Significant moderated mediation models revealed indirect effects of violence exposure on increasing depression over time through hippocampal and amygdala volumes, particularly among youths who experienced more stressful life events.

          CONCLUSIONS

          These results provide novel evidence for reduced hippocampal and amygdala volumes as mechanisms of stress sensitization to depression following exposure to violence. These findings suggest that hippocampal and amygdala-mediated emotional and cognitive processes may contribute to vulnerability to stressful life events following childhood violence exposure.

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          Author and article information

          Journal
          bioRxiv
          October 08 2019
          Article
          10.1101/798033
          871a8744-78dd-4718-ac36-3af0954f35f3
          © 2019
          History

          Molecular medicine,Neurosciences
          Molecular medicine, Neurosciences

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