Cognitive reappraisal is associated with major depressive disorder (MDD), while spontaneous activity patterns of the default mode network (DMN) is implicated in reappraisal and MDD. However, neural mechanisms subserving the close association of spontaneous reappraisal and depression are unclear. Spontaneous reappraisal, depression and resting-state functional magnetic resonance imaging (rsfMRI) were measured from 105 healthy subjects. We assessed the temporal complexity (Hurst exponent), Regional Homogeneity (ReHo) and fractional Amplitude of Low Frequency Fluctuation (fALFF) profiles of DMN, a network involved in both reappraisal and depression. Mediation effects of these standard measures on the relationship between reappraisal and depression, and the contributions of each DMN subregion, were assessed. Results indicated that Hurst exponent (H) of DMN, whether extracted by independent component analysis (ICA) or region of interest (ROI), was significantly associated with reappraisal scores. An individual with a higher reappraisal score has a lower Hurst value of DMN. Mediation analyses suggest that H of DMN partially mediates the association between reappraisal and the degree of depression, and this mediation effect arises from the contribution of medial prefrontal cortex. Neither ReHo nor fALFF showed a similar correlation or mediation effect. These findings suggest that temporal dynamics of DMN play an important role in emotion regulation and its association with depression. H of DMN may serve as a neural marker mediating the association between reappraisal and depression.
The link between cognitive function and emotion regulation may be helpful in better understanding the onset, maintenance, and treatment for depression. However, it remains unclear whether there are neural correlates between emotion dysregulation and cognitive deficits in depression. To address this question, we first review the neural representations of emotion dysregulation and cognitive deficits in depression (including deficits in cognitive control and cognitive biases). Based on the comparisons of neural representations of emotion dysregulation versus cognitive deficits, we propose an accessible and reasonable link between emotion dysregulation, cognitive control, and cognitive biases in depression. Specifically, cognitive control serves the whole process of emotion regulation, whereas cognitive biases are engaged in emotion regulation processes at different stages. Moreover, the abnormal implementation of different emotion regulation strategies in depression is consistently affected by cognitive control, which is involved in the dorsolateral, the dorsomedial prefrontal cortex, and the anterior cingulate cortex. Besides, the relationship between different emotion regulation strategies and cognitive biases in depression may be distinct: the orbitofrontal cortex contributes to the association between ineffective reappraisal and negative interpretation bias, while the subgenual prefrontal cortex and the posterior cingulate cortex underline the tendency of depressed individuals to ruminate and overly engage in self-referential bias. This review sheds light on the relationship between cognitive deficits and emotion dysregulation in depression and identifies directions in need of future attention.
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