Suicidal ideation (SI) is very common in patients with major depressive disorder (MDD). However, its neural mechanisms remain unclear. The anterior cingulate cortex (ACC) region may be associated with SI in MDD patients. This study aimed to elucidate the neural mechanisms of SI in MDD patients by analyzing changes in gray matter volume (GMV) in brain structures in the ACC region, which has not been adequately studied to date.

According to the REST-meta-MDD project, this study subjects consisted of 235 healthy controls and 246 MDD patients, including 123 MDD patients with and 123 without SI, and their structural magnetic resonance imaging data were analyzed. The 17-item Hamilton Depression Rating Scale (HAMD) was used to assess depressive symptoms. Correlation analysis and logistic regression analysis were used to determine whether there was a correlation between GMV of ACC and SI in MDD patients.

MDD patients with SI had higher HAMD scores and greater GMV in bilateral ACC compared to MDD patients without SI (all p < 0.001). GMV of bilateral ACC was positively correlated with SI in MDD patients and entered the regression equation in the subsequent logistic regression analysis.

Our findings suggest that GMV of ACC may be associated with SI in patients with MDD and is a sensitive biomarker of SI.

Major depressive disorder (MDD) is one of the most prevalent and disabling illnesses worldwide. Treatment of MDD typically relies on trial-and-error to find an effective approach. Identifying early response-related biomarkers that predict response to antidepressants would help clinicians to decide, as early as possible, whether a particular treatment might be suitable for a given patient.

Data were from the two-stage Establishing Moderators and Biosignatures of Antidepressant Response for Clinical Care (EMBARC) trial. A whole-brain, voxel-wise, mixed-effects model was applied to identify early-treatment cerebral blood flow (CBF) changes as biomarkers of treatment response. We examined changes in CBF measured with arterial spin labeling 1-week after initiating double-masked sertraline/placebo. We tested whether these early 1-week scans could be used to predict response observed after 8-weeks of treatment.

Response to 8-week placebo treatment was associated with increased cerebral perfusion in temporal cortex and reduced cerebral perfusion in postcentral region captured at 1-week of treatment. Additionally, CBF response in these brain regions was significantly correlated with improvement in Hamilton Depression Rating Scale score in the placebo group. No significant associations were found for selective serotonin reuptake inhibitor treatment.

We conclude that early CBF responses to placebo administration in multiple brain regions represent candidate neural biomarkers of longer-term antidepressant effects.

Exploring the neural basis related to different mood states is a critical issue for understanding the pathophysiology underlying mood switching in bipolar disorder (BD), but research has been scarce and inconsistent.

Resting-state functional magnetic resonance imaging data were acquired from 162 patients with BD: 33 (hypo)manic, 64 euthymic, and 65 depressive, and 80 healthy controls (HCs). The differences of large-scale brain network functional connectivity (FC) between the four groups were compared and correlated with clinical characteristics. To validate the generalizability of our findings, we recruited a small longitudinal independent sample of BD patients (n = 11). In addition, we examined topological nodal properties across four groups as exploratory analysis.

A specific strengthened pattern of network FC, predominantly involving the default mode network (DMN), was observed in (hypo)manic patients when compared with HCs and bipolar patients in other mood states. Longitudinal observation revealed an increase in several network FCs in patients during (hypo)manic episode. Both samples evidenced an increase in the FC between the DMN and ventral attention network, and between the DMN and limbic network (LN) related to (hypo)mania. The altered network connections were correlated with mania severity and positive affect. Bipolar depressive patients exhibited decreased FC within the LN compared with HCs. The exploratory analysis also revealed an increase in degree in (hypo)manic patients.

Our findings identify a distributed pattern of large-scale network disturbances in the unique context of (hypo)mania and thus provide new evidence for our understanding of the neural mechanism of BD.