4.4 Article

Common and differential neural mechanisms underlying mood disorders

Journal

BIPOLAR DISORDERS
Volume 24, Issue 8, Pages 795-805

Publisher

WILEY
DOI: 10.1111/bdi.13248

Keywords

default-mode network; frontoparietal network; mood disorders; resting-state fMRI; salience network

Funding

  1. National Health and Medical Research Council (NHMRC) of Australia [APP1087560]
  2. Takeda Pharmaceutical Company
  3. COCKPI-T (Co-Create Knowledge for Pharma Innovatio)

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This study aimed to investigate common and shared neural mechanisms underlying mood disorders, as well as possible neural changes relating to illness chronicity. The study found that all three clinical groups had significantly lower connectivity compared to controls, and bipolar disorder group exhibited significant differences in certain connectivity features compared to the treatment-resistant depression group.
Background Despite homogenous clinical presentations between bipolar and unipolar disorders, there are distinct neurobiological differences. Chronicity of illness may be a factor impacting and sustaining certain neural features. The goal of this study was to investigate common and shared neural mechanisms underlying mood disorders, and possible sustained neural changes relating to illness chronicity by investigating a cohort of euthymic patients with bipolar disorder (BD), unipolar depression who had responded to treatment (treatment-sensitive depression, TSD), and a chronically treatment-resistant depressed (TRD) group. Methods One hundred and seventy-two participants (40 BD, 39 TSD, 40 TRD, and 53 age-gender-matched healthy controls) underwent resting-state fMRI scans. Seed-based and independent component analyses were performed to investigate group differences in resting-state connectivity between the four groups. Results All three clinical groups had significantly lower connectivity within the frontoparietal network (FPN) relative to controls. TRD and BD were significantly different from TSD (TRD, BD > TSD) but were not significantly different from each other. TRDs were also significantly different from both BD and TSD for salience network connectivity with the posterior cingulate (DMN) and the FPN with frontal pole (DMN). Additionally, the BD group exhibited greater DMN-FPN (sgACC-RDLPFC) connectivity relative to TRD, TSD, and controls, which was correlated with a previous number of depressive episodes, in the BD group only. Conclusions BD demonstrated shared and differential connectivity features relative to symptomatic TRD and euthymic TSD groups. The increased sgACC-RDLPFC connectivity in BD and its correlation with a number of depressive episodes could be a neural feature associated with illness chronicity.

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