Persisting negative thoughts are considered a hallmark feature of depression. Recent information-processing approaches have begun to uncover the underlying mechanisms of depressive rumination. Despite marked advances in this area, there is a lack of integration between psychopathology and cognitive (neuro)science research. We propose the "impaired disengagement" hypothesis as a unifying framework between both approaches. The core tenet of our model is that prolonged processing of self-referent material is due to impaired attentional disengagement from negative self-referent information. We discuss the empirical evidence for this framework and outline future ways in which the causal predictions of this model can be tested. The proposed framework can account for the effectiveness of various treatments for depression and may aid in devising new interventions to target depressive cognition.

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Attentional bias to negative information has been proposed to be a cognitive vulnerability factor for the development of depression. In 2 experiments, the authors examined mood-congruent attentional bias in dysphoria. In both experiments, dysphoric and nondysphoric participants performed an attentional task with negative, positive, and neutral word cues preceding a target. Targets appeared either at the same or at the opposite location of the cue. Overall, results indicate that dysphoric participants show maintained attention for negative words at longer stimulus presentations, which is probably caused by impaired attentional disengagement from negative words. Furthermore, nondysphoric participants maintain their attention more strongly to positive words. These results are discussed in relation to recent developments in the pathogenesis and treatment of depression.

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A neurobiological account of cognitive vulnerability for recurrent depression is presented based on recent developments of resting state neural networks. We propose that alterations in the interplay between task positive (TP) and task negative (TN) elements of the Default Mode Network (DMN) act as a neurobiological risk factor for recurrent depression mediated by cognitive mechanisms. In the framework, depression is characterized by an imbalance between TN-TP components leading to an overpowering of TP by TN activity. The TN-TP imbalance is associated with a dysfunctional internally-focused cognitive style as well as a failure to attenuate TN activity in the transition from rest to task. Thus we propose the TN-TP imbalance as overarching neural mechanism involved in crucial cognitive risk factors for recurrent depression, namely rumination, impaired attentional control, and cognitive reactivity. During remission the TN-TP imbalance persists predisposing to vulnerability of recurrent depression. Empirical data to support this model is reviewed. Finally, we specify how this framework can guide future research efforts.

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Depression has been linked with impaired executive control and specific impairments in inhibition of negative material. To date, only a few studies have examined the relationship between depressive symptoms and executive functions in response to emotional information.Using a new paradigm, the Affective Shift Task (AST), the present study examined if depressive symptoms in general, and rumination specifically, are related to impairments in inhibition and set shifting in response to emotional and non-emotional material. The main finding was that depressive symptoms in general were not related to inhibition. Set shifting impairments were only observed in moderate to severely depressed individuals. Interestingly, rumination was related to inhibition impairments, specifically when processing negative information, as well as impaired set shifting as reflected in a larger shift cost. These results are discussed in relation to cognitive views on vulnerability for depression.