Journal
JOURNAL OF PSYCHIATRIC RESEARCH
Volume 156, Issue -, Pages 570-578Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jpsychires.2022.10.070
Keywords
Depression; Rumination; Brooding; Neural signal variability; BOLD variability; Dorsolateral prefrontal cortex
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Funding
- National Institute of Mental Health [R01MH094478]
- University of Wisconsin-Madison Office of the Vice Chancellor for Research and Graduate Education
- Wisconsin Alumni Research Foundation
- University of Wisconsin-Madison Women in Science and Engineering Leadership Institute/The Office of the Provost
- National Institutes of Mental Health [K23MH113733]
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This study investigated the association between rumination subtypes and BOLD signal variability in depression, and found that higher levels of rumination were associated with lower prefrontal neural signal variability. This relationship was also related to depression history.
Rumination is a common feature of depression and predicts the onset and maintenance of depressive episodes. Maladaptive and adaptive subtypes of rumination contribute to distinct outcomes, with brooding worsening negative mood and reflection related to fewer depression symptoms in healthy populations. Neuroimaging studies have implicated several cortical midline and lateral prefrontal brain regions in rumination. Recent research indicates that blood oxygen level-dependent (BOLD) signal variability may be a novel predictor of cognitive flexibility. However, no prior studies have investigated whether brooding and reflection are associated with distinct patterns of BOLD signal variability in depression. We collected resting-state fMRI data for 79 women with different depression histories: no history, past history, and current depression. We examined differences in BOLD signal variability (BOLDSD) related to rumination subtypes for the following regions of interest previously implicated in rumination: amygdala, medial prefrontal, anterior cingulate, posterior cingulate, and dorsolateral prefrontal cortices (dlPFC). Rumination subtype was associated with BOLDSD in the dlPFC, with greater levels of brooding associated with lower BOLDSD in the dlPFC, even after controlling for depression severity. Depression history was related to BOLDSD in the dlPFC, with reduced BOLDSD in those with current depression versus no history of depression. These findings provide a novel demonstration of the neural circuitry associated with maladaptive rumination in depression and implicate decreased prefrontal neural signal variability in the pathophysiology of depression.
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