Transdiagnostic commonalities and differences in resting state functional connectivity of the default mode network in schizophrenia and major depression

Abstract

Schizophrenia and depression are prevalent psychiatric disorders, but their underlying neural bases remains poorly understood. Neuroimaging evidence has pointed towards the relevance of functional connectivity aberrations in default mode network (DMN) hubs, dorso-medial prefrontal cortex and precuneus, in both disorders, but commonalities and differences in resting state functional connectivity of those two regions across disorders has not been formally assessed. Here, we took a transdiagnostic approach to investigate resting state functional connectivity of those two regions in 75 patients with schizophrenia and 82 controls from 4 scanning sites and 102 patients with depression and 106 controls from 3 sites. Our results demonstrate common dysconnectivity patterns as indexed by a significant reduction of functional connectivity between precuneus and bilateral superior parietal lobe in schizophrenia and depression. Furthermore, our findings highlight diagnosis-specific connectivity reductions of the parietal operculum in schizophrenia relative to depression. In light of evidence that points towards the importance of the DMN for social cognitive abilities and well documented impairments of social interaction in both patient groups, it is conceivable that the observed transdiagnostic connectivity alterations may contribute to interpersonal difficulties, but this could not be assessed directly in our study as measures of social behavior were not available. Given the operculum's role in somatosensory integration, diagnosis-specific connectivity reductions may indicate a pathophysiological mechanism for basic self-disturbances that is characteristic of schizophrenia, but not depression.

Resting-State Magnetoencephalography Reveals Different Patterns of Aberrant Functional Connectivity in Combat-Related Mild Traumatic Brain Injury

“…One expected consequence of DAI in WM is the disruption of neuronal communication among GM areas, which may lead to decreased FC with other brain regions, especially if axonal damage is substantial. For example, reduced FC is consistently found in patients with Alzheimer's disease and schizophrenia, [102][103][104][105][106] wherein structural changes in WM tissue are also found. [107][108][109][110][111][112] Therefore, the DAI model can explain the abnormally decreased FC in the right frontal pole in the present study.…”

Default mode functional connectivity is associated with social functioning in schizophrenia.

“…Many studies that evaluated resting-state DMN connectivity in schizophrenia using pICA reported on the connectivity between the main DMN hubs and other brain networks (Alonso-Solís et al, 2015; Jafri et al, 2008; Liang et al, 2006; Ongur et al, 2010; Zhou et al, 2007). Of the studies examining DMN connectivity (Alonso-Solís et al, 2015; Chang et al, 2014; Jafri et al, 2008; Li et al, 2015; Liang et al, 2006; Liemburg et al, 2012; Mingoia et al, 2012; Ongur et al, 2010; Schilbach et al, 2016; Zhou et al, 2007), only two studies directly examined connectivity between the DMN hubs (Chang et al, 2014; Liemburg et al, 2012). One of these studies found that individuals with schizophrenia exhibited decreased DMN inter-network connectivity as compared to controls (Liemburg et al, 2012), and one study did not observe group differences in DMN inter-network connectivity (Chang et al, 2014).…”

Adjunct ketamine treatment effects on treatment-resistant depressive symptoms in chronic treatment-resistant schizophrenia patients are short-term and disassociated from regional homogeneity changes in key brain regions – a pilot study

“…We postulated that this seemingly contradictory finding may be related to neuropathological features of schizophrenia. Indeed the neuropathological features of depressive symptoms in patients diagnosed with major depressive disorder have been reported to differ from those of depressive symptoms in patients with schizophrenia [69][70][71]. Hence, we posit that ketamine-induced ReHo alterations in schizophrenics may also be different from those in patients with major depressive disorder.…”