Imaging Functional Systems in Depression

Potential structural trait markers of depression in the form of alterations in the structures of subcortical nuclei and structural covariance network properties

“…These alterations may eventually contribute to the subcortical SCN changes in different stages of depression. From our results, the exploration for brain structural-based the complex relationship between morphology and topological properties may provide information for understanding the complex relationship between structural and functional network ( Honey et al, 2007 , Rubinov and Sporns, 2010 ) in the neurobiological mechanisms of depression ( Disner et al, 2011 , Pagliaccio and Barch, 2016 , Young et al, 2016 ). Although previous studies showed that structure and function were highly correlated, this correspondence was imperfect ( Honey et al, 2009 ) because function reflects the complex multi-synaptic interactions in the structural network ( Suárez et al, 2020 ).…”

“…Although altered topological SCN properties of cortical regions have been reported in a previous study of depression ( Wang et al, 2016 ), the present study only focused on the subcortical structures. Trait marker, state-dependent marker, and SCN data for subcortical structures thus would provide new evidence to contribute to the elucidation of neurobiological mechanisms of depression ( Beck and Bredemeier, 2016 , Disner et al, 2011 , Drevets et al, 2008 , Young et al, 2016 ).…”

“…The information about negative stimuli is to be sent to a subcortical circuit, including the hippocampus, for additional processing, and then finally to a cortical circuit where self-referential schemas and rumination are induced, thus promoting depressive symptoms. Furthermore, a group of subcortical nuclei (the main components of the basal ganglia), including the caudate, putamen, NAc, and pallidum have been reported to play a critical role in core physiological depressive symptoms, such as psychomotor symptoms ( Buyukdura et al, 2011 ) and anhedonia ( Berridge and Kringelbach, 2015 , Smith et al, 2009 , Young et al, 2016 ). Although recent studies reported GMVs alterations in multiple subcortical structures of MDD patients ( Koolschijn et al, 2009 , Lu et al, 2016 , Nugent et al, 2013 , Schmaal et al, 2016 ) and no significant GMVs alterations in subcortical regions of RD patients ( Arnold et al, 2012 ), yet most studies did not include patients with RD, making it difficult to explore the potential subcortical MDD trait markers.…”

Gray matter structures associated with neuroticism: A meta‐analysis of whole‐brain voxel‐based morphometry studies

“…It has been proposed that neuroticism is driven by an increased tendency for generating self‐referential cognition, especially negative thoughts (Perkins et al, 2015), and recall of negative real‐life events (i.e., autobiographical memory; Denkova, Dolcos, & Dolcos, 2012), which is associated with structural integrity and activity changes in the mPFC (Bernhardt et al, 2014; Smallwood & Schooler, 2015). Further, aberrant DMN activity and mPFC‐ACC connectivity are related to rumination (i.e., the repetitive and negative self‐referential processing) in depression (Hamilton et al, 2011; Young, Mueller, & Tendolkar, 2016), which exhibits strong link with neuroticism (Jeronimus et al, 2016; Kotov et al, 2010). In a treatment study, subjects scored higher on neuroticism showed decreased activity in the dACC/mPFC in response to negative self‐referential processing in a word categorization task after administration of antidepressant (Di Simplicio, Norbury, & Harmer, 2012) than those receiving placebo.…”