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Conclusions: In addition to exacerbating daily suicidality, ovarian steroid withdrawal both natural perimenstrual and experimental withdrawal provoked heightened sadness, hopelessness, anhedonia, impulsivity, social disconnection, and trouble sleeping in a sample of female suicide attempters with current suicidal ideation. Anxiety was not affected and may not be a key mechanism.

Studies should probe whether disturbed sleep may represent a mechanism between steroid withdrawal and psychiatric symptoms. Perhaps due to shared risk factors, chronic suicidality in females seems to correlate with psychiatric sensitivity to perimenstrual steroid withdrawal. This withdrawal mechanism stands in contrast to those observed in premenstrual dysphoric disorder, where symptoms are triggered by post-ovulatory neurosteroid changes rather than perimenstrual steroid changes.

Serum from the present study is currently being assayed to examine possible molecular mechanisms, such as GABAergic neurosteroid withdrawal.

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Remediating the face emotion recognition deficit could 1 reduce depressed mood in people with BD, 2 improve social functioning, and 3 increase treatment engagement. Previous research has indicated that a computer-based cognitive bias modification intervention designed to modify emotion perception biases may positively influence mood and behavior in depressed and aggressive individuals Penton-Voak et al.

Our goals are to determine whether this intervention can shift emotion processing biases in people with BD and demonstrate clinical benefits lower depressed mood, improved social function, greater treatment engagement.

Exclusion criteria were minimal. Participants were interviewed to assess eligibility and completed mood and social functioning self-reports. Participants were randomized to the active or sham condition. Results: Forty-three participants average age There were no main effects for group, time, or their interaction on mania scores or treatment status initiating medication or participating in psychotherapy. Among those participants who underwent neuroimaging pre- and post-intervention, at baseline there was significant activation in the dorsal medial prefrontal cortex DMPFC when observing the emotional faces happy, sad.

Following the intervention, there was no significant activation in this area. A reduction in DMPFC response after intervention provides preliminary support for it as a neural treatment target and is consistent with its role in emotion regulation, identification, and learning Bakker et al. These results converge with prior work demonstrating IBT may reduce depressed mood in healthy individuals Penton-Voak et al. On average, people with BD spend more time depressed than manic, and depressed mood tends to be more difficult to treat Baldessarini et al.

Importantly, this computer-based intervention can be more easily disseminated, at lower cost, than traditional interventions, creating an opportunity to benefit under-served populations. Background: Little is known about the neural substrates of suicide risk in mood disorders. Improving the identification of biomarkers of suicide risk in mood disorders could lead to more targeted treatments to reduce risk.

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The aim of this study was to use resting-state intrinsic network connectivity to identify individuals at risk for suicide, as indicated by a history of suicide-related behavior SB. Methods: A cross-sectional study was conducted at two urban communities with medical centers. Resting-state functional connectivity was examined within intrinsic networks, including the cognitive control network CCN , a system involving frontoparietal and dorsal attention networks that is critical for problem-solving and executive functioning; the salience and emotional network SEN , which is active in response to stimuli relevant to current goals, including emotional stimuli, and involves limbic and ventral attention networks; and the default mode network DMN , which is active during self-focused thought and when not engaged with external stimuli.

Two fMRI scans were conducted approximately two months apart to examine stability and reliability of group differences over time. Intrinsic network connectivity effects were stable over time and identified group membership with good accuracy, sensitivity, and specificity. Conclusions: These results suggest that individuals with a history of SB may show distinct patterns of intrinsic network connectivity, even when compared to those with mood disorders and no history of SB.

These deficits may underlie candidate behavioral risk factors for suicidal ideation and suicidal behavior, including rumination and inhibitory control deficits. Resting-state fMRI may serve as a promising tool for identifying subtypes of patients with mood disorders who are at risk for suicidal behavior. Background: Adolescence is a developmental period in which depression and related mood syndromes often emerge.

However, few objective markers exist to guide diagnosis or predict mood health in youth. The present study addressed this gap using task-based neuroimaging to identify frontoinsular biomarkers of current and prospective mood health in adolescents. Analyses tested associations between task-related functional connectivity in frontoinsular networks involved in attention regulation, and baseline or prospective measures of mood health.

Sex was considered as a biological variable of interest. In particular, task-related hypoconnectivity between insula and lateral prefrontal regions of the frontoparietal network, and hyperconnectivity between insula and midline or temporal regions of the default network, were associated with poorer mood health.

Prospective associations between frontoinsular functioning and mood health were significant when controlling for baseline symptoms, indicating that biomarkers complement other sources of risk information. Conclusions: Findings for frontoinsular imbalances as a biomarker of current and prospective mood health in adolescence suggest that network functioning may hold promise as a translational tool to guide risk prediction and inform preventive treatments. Background: Electroconvulsive therapy is the most effective treatment for major depressive disorder MDD.

The understanding of the neurobiological mechanism underlying ECT efficacy remains incomplete. Previous studies have reported ECT-induced changes in multiple neurotransmitter systems, including the serotonin 5-hydroxy-tryptamine, 5-HT system. Serotonin has been shown to modulate various physiological processes, such as thermoregulation, and behavioral functions, such as the sleep-wake cycle, aggression, mood and anxiety, sexual behavior, and learning.

Thus, pathological changes of central serotonergic neurotransmission are associated with an array of psychiatric conditions, including MDD. Growing evidence suggests that LDAEP may be biological markers for predicting response to antidepressants. Nine patients with MDD 6 female, age Patients received a standard course of ultrabrief pulse width right unilateral ECT.

MEG was recorded using the Elektra Neuromag VectorView system, equipped with magnetometers and planar gradiometers, in addition to electrocardiography and electrooculography recordings. Brainstorm 3 was used for MEG data processing and visualization. Individual head models were reconstructed from structural MRI using Freesurfer, and coregistered to the scalp fiducials.

Faulty channels were manually removed. Heartbeat and eyeblink artifacts were removed using signal-space projection method. Independent component analysis was used to remove additional non-brain artifact. Source reconstruction was done using the linearly constrained minimum variance LCMV beamformer method.

The trial-averaged, source-level, event-related field ERF was extracted from the bilateral primary auditory cortices PAC of each subject. The change in ERF amplitude between the N and P peaks was extracted and plotted as a function of tone intensity, the slope of the linear fit defines the loudness dependence of the auditory evoked potential.

Conclusions: Contrary to our hypothesis, the results indicate a greater dependence of auditory evoked potential on loudness levels after the ECT treatment course. This leads us to an alternative hypothesis, that the antidepressant effects of ECT are in part mediated by increased dopamine neurotransmission, which has been shown in a previous study to be positively associated with increased LDAEP. Background: Patient response to antidepressant varies greatly, likely contributed by multiple factors, including mutations, altered signaling and metabolic pathways.

This project aimed to integrate DNA, microRNA and mRNA data to discover molecular pathways associated with treatment response to antidepressants using an integrated network analysis approach. Results: Analysis of individual data sources yielded no significant results; however, network-based analysis across microRNA, RNA and DNA samples identified 1, significantly enriched pathways.

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Immune signaling pathways emerged as the most significant pathways both individually and upon systematic domain specific classification. The top immune signaling pathways were then successfully validated for differential expression among predicted responders to duloxetine. Conclusions: The results confirmed currently implicated pathways and pointed towards novel pathways for further exploration.

In particular, specific pathways such as TRAF6 emerged as key players in antidepressant treatment response to duloxetine. Within the validated immune signaling pathways could exist proteins that serve as unique molecular targets to decipher the biology of antidepressant treatment response. The integrative network analysis approach demonstrates that variations of a small effect size at the molecular level can aggregate within pathways that could be meaningfully explored and targeted in antidepressant response.

Background: Numerous clinical studies have provided strong evidence that ketamine rapidly within hours of administration improves depressive symptoms in treatment-resistant depressed patients following a single infusion. Our data also support a role of enhanced high-frequency EEG activity as a marker of target engagement and synaptic activity, which underlie rapid antidepressant efficacy. Background: Heat shock proteins HSPs are ubiquitously expressed intracellular proteins that function as chaperones and assist in the synthesis and folding of proteins in the absence of stress.

However, both animal models and human data suggest that HSPs are robustly upregulated in response to physical, cellular, and psychological stress. While intracellular HSP expression aids in the repair and stabilization of proteins during stress, the passive during necrosis or apoptosis or active release of these proteins into the extracellular matrix leads to increased production of pro-inflammatory cytokines.

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Of the known HSPs that mediate inflammatory response to stress, HSP70 has been implicated in psychiatric disorders, including major depressive disorder MDD ; indeed, multiple studies have shown increased HSP70 serum levels in patients at risk for or diagnosed with MDD. Other studies have found that increased HSP70 levels correlate strongly with symptom severity in patients with chronic negative affect.

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This study sought to investigate whether the glutamatergic regulator ketamine affects the expression of HSP70 in individuals with treatment-resistant MDD. Methods: This double-blind, placebo-controlled, randomized, crossover study included 38 medication-free males and females with MDD and 23 healthy controls HCs ages between years old.

Ketamine and placebo infusions were administered two weeks apart; the study was designed to test the antidepressant efficacy of ketamine. Initial leads for the HSP70 were obtained from an initial pilot proteomic study of looking at MDD patient that are extreme ketamine responders, non-responders and the HCs individuals. Age, sex, and body mass index were used as covariates. Thus, while ketamine decreased the severity of depressive symptoms, this change did not appear to be mediated by changes in HSP70 levels. Conclusions: These preliminary findings suggest that ketamine affects HSP70 levels by decreasing stress and inflammation.

Additional hypothesis-driven mechanistic studies designed to test the impact of subanesthetic ketamine on HSP70 expression are needed to further explore this initial finding. Background: Women are approximately two times as likely to be diagnosed with major depressive disorder MDD compared to men. These sex differences in MDD might be driven by circulating gonadal hormone differences between men and women. Indeed, both female and male gonadal hormones influence mood in humans e.

However, MDD prevalence remains higher in women across life stages and hormonal states, suggesting that other sex-related factors contribute to higher rates of MDD in women. Mice were gonadectomized in adulthood to eliminate circulating hormone effects and isolate the role of developmental hormones.