A supplementary functional connectivity microstate attached to the default mode network in depression revealed by
Siqi Zhang1, Shui Tian1, Mohammad Ridwan Chattun2
1School of Biological Sciences & Medical Engineering, Southeast University, Nanjing 210096, China; Key Laboratory of Child Development and Learning Science, Southeast University, Nanjing 210096, China.
Abstract:
Default mode network (DMN) has discernable involvement in the representation of negative, self-referential information in depression. Both increased and decreased resting-state functional connectivity between the anterior and posterior DMN have been observed in depression. These conflicting connectivity differences necessitated further exploration of the resting-state DMN dysfunction in depression. Hence, we investigated the time-varying dynamic interactions within the DMN via functional connectivity microstates in a sub-second level. 25 patients with depression and 25 matched healthy controls were enrolled in the MEG analysis. Spherical K-means algorithms embedded within an iterative optimization frame were applied to sliding windowed correlation matrices, resulting in sub-second alternations of two functional connectivity microstates for groups and highlighting the presence of functional variability. In the power dominant state, depressed patients showed a transient decreased pattern that reflected inter/intra-subnetwork deregulation. A supplementary negatively correlated state simultaneously presented with increased connectivity between the ventromedial prefrontal cortex (vmPFC) and the posterior cingulate cortex (PCC), two core nodes for the anterior and posterior DMN respectively. Additionally, depressed patients stayed longer in the supplementary microstate compared to healthy controls. During the time spent in the supplementary microstate, an attempt to compensate for the aberrant effect of vmPFC on PCC across DMN subnetworks was possibly made to balance the self-related processes disturbed by the dominant pattern. The functional compensation mechanism of the supplementary microstate attached to the dominant disrupted one provided a possible explanation to the existing inconsistent findings between the anterior and posterior DMN in depression.
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