Depression during and after pregnancy affects up to 20% of pregnant women, but the biological underpinnings remain incompletely understood. As pregnancy progresses, the immune system changes to facilitate fetal development, leading to distinct fluctuations in the production of pro-inflammatory factors and neuroactive tryptophan metabolites throughout the peripartum period. Therefore, it is possible that depression in pregnancy could constitute a specific type of inflammation-induced depression. Both inflammatory factors and kynurenine metabolites impact neuroinflammation and glutamatergic neurotransmission and can therefore affect mood and behavior. To determine whether cytokines and kynurenine metabolites can predict the development of depression in pregnancy, we analyzed blood samples and clinical symptoms in 114 women during each trimester and the postpartum. We analyzed plasma IL-1β, IL-2, -6, -8, -10, TNF, kynurenine, tryptophan, serotonin, kynurenic- quinolinic- and picolinic acids and used mixed-effects models to assess the association between biomarkers and depression severity. IL-1β and IL-6 levels associated positively with severity of depressive symptoms across pregnancy and the postpartum, and that the odds of experiencing significant depressive symptoms increased by >30% per median absolute deviation for both IL-1β and IL-6 (both P = 0.01). A combination of cytokines and kynurenine metabolites in the 2nd trimester had a >99% probability of accurately predicting 3rd trimester depression, with an ROC AUC > 0.8. Altogether, our work shows that cytokines and tryptophan metabolites can predict depression during pregnancy and could be useful as clinical markers of risk. Moreover, inflammation and kynurenine pathway enzymes should be considered possible therapeutic targets in peripartum depression.

Objective Computerized adaptive tests (CAT) provide an alternative to fixed-length assessments for diagnostic screening and severity measurement of psychiatric disorders. We sought to cross-sectionally validate a suite of computerized adaptive tests for mental health (CAT-MH) in a community psychiatric sample. Methods 145 adult psychiatric outpatients and controls were prospectively evaluated with CAT for depression, mania and anxiety symptoms, compared to gold-standard psychiatric assessments including: Structured Clinical Interview for DSM IV-TR (SCID), Hamilton Rating Scale for Depression (HAM-D25), Patient Health Questionnaire (PHQ-9), Center for Epidemiologic Studies Depression Scale (CES-D), and Global Assessment of Functioning (GAF). Results Sensitivity and specificity for the computerized adaptive diagnostic test for depression (CAD-MDD) were .96 and .64, respectively (.96 and 1.00 for major depression versus controls). CAT for depression severity (CAT-DI) correlated well to standard depression scales HAM-D25 (r=.79), PHQ-9 (r=.90), CES-D (r=.90) and had OR=27.88 for current SCID major depressive disorder diagnosis across its range. CAT for anxiety severity (CAT-ANX) correlated to HAM-D25 (r=.73), PHQ-9 (r=.78), CES-D (r=.81), and had OR=11.52 for current SCID generalized anxiety disorder diagnosis across its range. CAT for mania severity (CAT-MANIA) did not correlate well to HAM-D25 (r=.31), PHQ-9 (r=.37), CES-D (r=.39), but had an OR=11.56 for a current SCID bipolar diagnosis across its range. Participants found the CAT-MH suite of tests acceptable and easy to use, averaging 51.7 items and 9.4 minutes to complete the full battery. Conclusions Compared to current gold-standard diagnostic and assessment measures, CAT-MH provides an effective, rapidly-administered assessment of psychiatric symptoms.

Background: Suicide risk assessments are often challenging for clinicians, and therefore, biological markers are warranted as guiding tools in the assessments. Suicidal patients display increased cytokine levels in peripheral blood, although the composite inflammatory profile in the subjects is still unknown. It is also not yet established whether certain inflammatory changes are specific to suicidal subjects. To address this, we measured 45 immunobiological factors in peripheral blood and identified the biological profiles associated with cross-diagnostic suicide risk and depression, respectively.

SAA might constitute a cross-diagnostic marker indicative of depressed mood and fatigue in a naturalistic patient setting. Because SAA activates Toll-like receptors 2 and 4, present on macrophages and glial cells, its association with depression severity could also implicate this inflammatory mediator in the pathogenesis of mood disorders.

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