Neural Correlates of Proactive Control in Major Depressive Disorder

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Depression is a mental disorder with high lifetime prevalence and enormous societal costs. Cognitive deficits in depression have been observed numerous times. Previous studies have reported well-replicated deficits in cognitive control, i.e. the flexible, goal-oriented control of basic cognitive and motor processes. Particularly important in this context are findings which demonstrate that performance in cognitive control can be influenced by the affective valence of the utilised stimuli. For example, deficits in cognitive control in depression have been found to be particularly strong when negatively valenced information has to be processed. These findings are of importance not only as they help to improve our understanding of the mechanisms of cognitive deficits in depression; they also provide an important basis for further development of cognitive behavioural therapy approaches. In this application, we propose two studies to be run in parallel in Bonn (Ettinger) and Tirol (Duschek), in order to substantially extend prior research in this area. First, we aim to integrate the study of cognitive control in depression into the theoretical framework of the Dual Mechanisms of Control Model by Braver (2012). This model, which has proven influential in cognitive psychology and cognitive neuroscience research, distinguishes between proactive and reactive modes of control and allows making predictions regarding selective impairments in those aspects of control in mental disorders. Second, we aim to systematically study the influence of affective modulation on proactive control. Finally, we wish to characterise the neural correlates of these processes; in Bonn we proposed to use functional magnetic resonance imaging (fMRI) and in Tirol we will use electroencephalography (EEG). In Study I (Bonn), 50 outpatients with a DSM 5 diagnosis of depression and 50 healthy controls (m/f) will perform an inhibitory control task (antisaccades) in fMRI. Proactive control in the inhibition of saccades will be modulated through the application of emotionally negative (angry, fearful, sad faces), positive and neutral stimuli. In Study II (Tirol), the antisaccade task will be applied simultaneously with recordings of event-related potentials in 50 outpatients with depression and 50 healthy controls (m/f). Overall, the two studies will provide a comprehensive and detailed characterisation of proactive cognitive control in depression, its modulation by affective factors and its neural correlates. The two studies ideally complement each other in terms of the selected aspects of cognitive control and the chosen neuroscientific methods, which allow investigation of both spatial (fMRI) and temporal (EEG) aspects of the neural correlates of proactive control.