Decreased hedonic and motivational capacity, namely anhedonia, is one of the cardinal features for patients with major depressive disorder (MDD). Recent studies suggest that this reduced ability to experience pleasure is also a marker or endophenotype for MDD and represents a genetic predisposition to this disorder.

Dr. CHAN Raymond from the Institute of Psychology of Chinese Academy of Sciences, and his collaborator, Dr. LIU Wenhua from Guangzhou Medical University, have previously shown that individuals with MDD and subsyndromal depression have difficulty in sustaining behavior during a known reinforcement schedule. These individuals are less likely to sustain behavior to optimize reward under stress. However, very little is known about the mechanisms underlying this heightened risk in unaffected first-degree relatives of patients with MDD.

In a recent study, Drs. CHAN and LIU and their international collaborator, Prof. ROISER Jonathan from University College London, have conducted study to examine the development of reward bias in 47 unaffected first-degree relatives of patients with MDD and 60 healthy controls. The researchers administered the same set of paradigm and measures they used in the previous study, a probability reward difficult visual discrimination task and self-reported measures of anhedonia and depression.

In the probability reward difficult visual discrimination task, participants were instructed about the contingencies in order to elicit a response bias towards the more frequently rewarded stimulus, termed as “reward bias”. The unaffected relatives were further classified to individuals with and without subsyndromal depression (depending on the self-reported measure of depression). Their findings showed that these unaffected first-degree relatives of patients with MDD with subsyndromal depression displayed a blunted reward bias comparing to healthy controls.

Those relatives without subsyndromal depression displayed largely intact motivational processing on both self-report and experimental measures. The severity of anhedonia was also correlated with attenuated reward bias in first-degree relatives of patients with MDD, especially in those with subsyndromal depression.

Taken together, the findings suggest that a subgroup of unaffected first-degree relatives of patients with MDD can be identified to show reward bias and anhedonia similar to patients with MDD. This subgroup was characterized by the presence of subsyndromal depressive symptoms. Moreover, blunted reward sensitivity may constitute a risk marker for MDD. The findings highlighting the existing clinical characterization of anhedonia in depression may represent an aggression of several underlying cognitive constructs and requires further refinement in clinical practice.

This study was supported by a grant from the Strategic Priority Research Programme (B) of Chinese Academy of Sciences, National Science Foundation of China, the Beijing Training Project for the Leading Talents in S & T, the Key Laboratory of Mental Health, Institute of psychology of Chinese Academy of Sciences, the Guangzhou Education Bureau, Project of Humanities and Social Sciences of Guangdong Province, and MOE Foundation of Humanities and Social Sciences.

The paper is available online in Journal of Affective Disorders.