Figure 7.1

SENSO framework showing biological, cognitive, neural, and behavioral responses following social rejection or threat of rejection.

Legend: SAM: sympathetic adrenal medullary; vACC: ventral anterior cingulate; DMN: default mode network; dACC: dorsal anterior cingulate; VLPFC: ventrolateral prefrontal cortex; DLPFC: dorsolateral prefrontal cortex; HPA: hypothalamic–pituitary–adrenocortical axis.

We suggest that the integrated and coordinated set of responses following social rejection signals are impaired in MDD, resulting in an abnormal homeostatic state of social acceptance, an increased sensitivity to social signals, and maladaptive behaviors in MDD. We are now currently testing in our laboratory the SENSO framework in MDD.

Preliminary evidence suggests that there is an increased sensitivity to social rejection in individuals with MDD. For example, self-esteem modulates the reactivity to social rejection and it is well documented that individuals at risk for and currently affected by MDD report lower self-esteem (Franck & Deraedt, 2007). In a recent fMRI study in which subjects received feedback from peers on how they were liked or disliked, Somerville and colleagues (Somerville, Kelley, & Heatherton, 2010) showed that the level of self-esteem modulates reactivity of the ventromedial prefrontal cortex to positive and negative social feedback (Onoda et al., 2010). Decreased self-esteem induced by social exclusion may affect self-evaluation and increase self-focused attention (“Am I likable? Why others do not like me?”) as commonly observed in MDD.

In adolescents, Masten and colleagues (Masten et al., 2011) have shown that the level of activation of the subgenual anterior cingulate after exposure to a cyberball task predicts, at one-year follow-up, the occurrence of depression. Consistent with this finding, in a recent meta-analysis of fMRI studies of social rejection, we observed that social rejection was associated with increased activity in the same subgenual part of the cingulate cortex (Rotge et al., 2015), a key region involved in the pathophysiology of MDD.

Finally, Davey and colleagues (Davey, Allen, Harrison, & Yücel, 2011), using a new cognitive task where subjects received positive social feedback from strangers who evaluated them, found an increased amygdala activation in young people with MDD. Taken together, patients with MDD have demonstrated that they also experience heightened sensitivity to positive social signals, suggesting a non-specific arousal to social stimuli that are misinterpreted as aversive.

Conclusion

In this chapter we have reviewed evidence on impaired social cognitive processes in MDD. Major depressive disorder affects several cognitive processes including, but not limited to, perception of basic social signal, self and other representation, and monitoring of social acceptance and social inclusion. An overlap between the emotional brain and social brain exists; therefore, the study of social cognition may provide new pathophysiological pathways in MDD. Applying a social neuroscience perspective on MDD represents a promising and innovative development, having the power to yield functional biomarkers and defining new therapeutic targets for MDD (e.g. prosocial agents such as oxytocin).

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