Alterations in cognitive and emotional brain networks related to depression

Abstract

It is essential for social interactions if one can process the perceived external world with appropriate cognitive control and well-regulated emotion. However, compared with healthy individuals, patients with major depression disorder (MDD) usually exhibit compromised cognitive and enhanced emotional processes, respectively; and these behavioral changes have been shown to be associated with alterations in functional brain networks. Recent advances of MDD research have been increasingly involving functional magnetic resonance imaging (fMRI) and focusing on brain networks of cognition and emotion, as well as the interaction of these two networks. While inconsistencies and debates noted, the present paper attempts to review and provide a summarized finding for these recent fMRI studies. Converging results have shown that MDD is associated with significant alterations in the fronto-limbic system. Specifically, compared with healthy controls, individuals with MDD usually show hyperactivation to negative facial stimuli in the amygdala, reflecting increased withdrawal, the core syndrome of depression. Some studies have also attempted to use hyperactivities of amygdala as the biomarker and reported its predictive value for MDD. Besides amygdala, increased insula response to disgusting faces was also reported in literature, emphasizing the role of disgust in emotional dysregulation. Cognitive abnormalities in depression mainly concern the default mode and executive control networks. In addition to alterations of regional activation in task state, individuals with MDD exhibit increased functional connectivity of the default mode network in resting state, suggesting enhanced self-referential processes. In particular, higher functional connectivity in the anterior default mode network corresponds with higher level of rumination. In the executive control network, many previous studies observed a decreased activation of dorsolateral prefrontal cortex in depression, indicating impaired ability of cognitive control. At the same time, recent research found that transcranial direct current stimulation in the left dorsolateral prefrontal cortex was helpful for working memory enhancement in individuals with MDD. While alterations were reported in the emotional and cognitive networks separately, interactive changes of these 2 modules have also been examined when they are simultaneously probed. Most studies have noted that when challenged with negative emotion, individuals with depression show increased activation in amygdala and decreased activation in dorsolateral prefrontal cortex, indicating a biased processing resource allocation towards the emotional system. Based on the aforementioned fMRI studies of MDD, we suggest that future improvements may consider aspects of (i) matching depressive syndromes for optimized confounding factor control; (ii) incorporating multimodal approaches for both brain imaging and stimulation; as well as (iii) applying neuroimaging together with psychological therapies either for prognosis evaluation or neurofeedback training.