Background: Anhedonia is a cardinal feature of major depression and is hypothesized to be driven by low motivation, in particular blunted reward sensitivity. It has been suggested to be a marker that represents a genetic predisposition to this disorder. However, little is known about the mechanisms underlying this heightened risk in unaffected first-degree relatives of patients with major depression. We previously demonstrated abnormal reward biases in acutely depressed patients. The present study aimed to examine the development of reward bias in first-degree relatives of patients with major depression.
Methods: Forty-seven first-degree relatives of patients with major depression (26 females, age 18-52) and 60 healthy controls with no family history of depression (34 females, age 21-48) were recruited. A probabilistically rewarded difficult visual discrimination task, in which participants were instructed about the contingencies, was used to assess blunted reward sensitivity. A response bias towards the more frequently rewarded stimulus (termed "reward bias") was the primary outcome variable in this study. Participants also completed self-reported measures of anhedonia and depressive symptoms.
Results: Compared with the control group, relatives of patients with major depression with sub-clinical depressive symptoms displayed a blunted reward bias. Relatives without symptoms displayed largely intact motivational processing on both self-report and experimental measures. The degree of anhedonia was associated with attenuated reward bias in first-degree relatives of patients with major depression, especially in those with sub-clinical symptoms.
Limitations: The study did not include a depressed patient group, which restricted our ability to interpret the observed group differences.
Conclusions: Blunted reward sensitivity may be largely manifested in a subgroup of relatives with high levels of depressive symptoms.
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http://dx.doi.org/10.1016/j.jad.2015.10.050 | DOI Listing |
Over the last decade, Hippo signaling has emerged as a major tumor-suppressing pathway. Its dysregulation is associated with abnormal expression of and -family genes. Recent works have highlighted the role of YAP1/TEAD activity in several cancers and its potential therapeutic implications.
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Department of Medicine, National University of Singapore, Yong Loo Lin School of Medicine, Singapore, Singapore.
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