Search

Background: Patients with depression show abnormalities in the neural circuitry supporting working memory. These abnormalities apparently persist into clinical remission, raising the possibility that they might be trait markers indicating vulnerability to depression. Methods: We studied 17 young people who had a depressed parent but no personal history of depressive illness (FH) and 15 healthy control subjects with no family history of depression. Participants performed a verbal working memory task of varying cognitive load (n-back) while undergoing functional magnetic resonance imaging scanning. We used multiple regression analyses to assess overall capacity (1-, 2-, 3-back vs. 0-back) as well as linear and quadratic modulation of cognitive demand. Results: Performance accuracy and response latency did not differ between groups, and overall capacity was similar. However, for both linear and quadratic load response activity, FH participants showed greater activation in lateral occipital cortex, superior temporal cortex, and superior parietal cortex. Conclusions: Our data suggest that, as in depressed patients, maintenance of task performance in FH participants is associated with a significant increase in the load-response activity of the cortical regions involved in working memory. This neural abnormality could form part of the predisposition to develop depressive disorders. [Copyright &y& Elsevier]

Abstract: Negative biases in emotional information processing are characteristic of patients with acute depression and may persist after clinical recovery. It is not clear, however, whether such biases are present before the onset of the depressive disorder. The aim of the present study was to examine whether young people at risk of depression, by virtue of having a depressed biological parent (FH+), demonstrate negative biases in tasks of emotional facial recognition and emotional categorization. We also assessed whether task performance and the influence of parental depression are modified by allelic variation in the serotonin transporter (5HTT) gene. We found that the FH+ participants did not show evidence of negative biases relative to matched controls. They were, however, significantly slower to perform a task of emotional categorization. 5HTT genotype did not influence emotional processing significantly. We conclude that negative biases in emotional processing do not appear to be present in people with a family history of depression. However, impairment in emotional categorization could identify a high-risk phenotype and may indicate that people at genetic risk of depression have difficulty in using “mood as information”. [Copyright &y& Elsevier]