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Background: The higher prevalence of major depressive disorder (MDD) in females relative to males is well-established. Some authors have posited this difference arises to divergent symptom profiles in females vs. males. However, empirical tests of this hypothesis have yielded equivocal results. Here, we investigate sex differences in MDD of individual symptoms and symptom networks in a treatment-seeking sample., Methods: We assessed depressive symptoms using Hamilton Depression Rating Scale (HDRS-17) in 590 treatment-seeking adults with MDD (300 females). We examined group differences in symptom endorsement. We investigated symptom networks and estimated Gaussian Graphical Models. Finally, we compared the female and male networks using the Network Comparison Test., Results: Females scored significantly higher in psychological anxiety (p <0.001; rB = -0.155), somatic anxiety (p = .001; rB = -0.150) and feelings of guilt (p = .002; rB = -0.139). Male and female patients did not differ in depression sum scores. There were no sex differences in network structure or global strength., Limitations: Our study was sufficiently powered to detect only medium sized symptom differences. The generalizability of our study is limited to clinical samples and further studies are needed to investigate if findings also translate to outpatient samples., Conclusion: Females reported elevated anxiety symptoms and guilt. Clinicians should assess these symptom differences and tailor treatment to individual symptom profiles. No differences between sexes emerged in MDD network structures, indicating that features may be more similar than previously assumed. Sex differences in psychopathological features of MDD are important for future research and personalized treatment., (Copyright © 2020. Published by Elsevier B.V.)

Introduction: Psychodynamic psychotherapy is an effective and widely used treatment for major depressive disorder (MDD); however, little is known about neurobiological changes associated with induced symptom improvement. Methods: Proton magnetic resonance spectroscopy with a two-dimensional J-resolved sequence served to test the relationship between glutamate (Glu) and glutamine (Gln) levels, measured separately in pregenual anterior cingulate cortex (pgACC) and the anterior midcingulate cortex (aMCC) as a control region, with change in depression symptoms after 6 months of weekly psychodynamic psychotherapy sessions in MDD patients. Depressed (N = 45) and healthy (N = 30) subjects participated in a baseline proton magnetic resonance spectroscopy measurement and a subgroup of MDD subjects (N = 21) then received once-a-week psychodynamic psychotherapy and participated in a second proton magnetic resonance spectroscopy measurement after 6 months. Change in depression symptoms was assessed using the Hamilton Depression Rating Scale (HAMD). Results: Higher pretreatment pgACC Gln concentrations in MDD patients compared to healthy controls were associated with symptom severity. Patients and controls did not differ regarding Gln levels in aMCC nor regarding Glu levels in both regions. The association of pgACC Gln concentration and severity of depressive symptoms was reversed after 6 months of psychotherapy in MDD subjects. Regarding Gln in aMCC as well as Glu in both regions, there were no significant associations with improvement of depressive symptoms in the course of psychotherapy. Discussion: Findings indicate specific regional effects of psychodynamic psychotherapy on glutamatergic neurotransmission and thereby highlight the key role of the pgACC in both depression pathophysiology and recovery. [ABSTRACT FROM AUTHOR]

A mechanism-based approach was developed focusing on the psychodynamic, psychological and neuronal mechanisms in healthy and depressed persons. In this integrative concept of depression, the self is a core dimension in depression. It is attributed to negative emotions (e.g., failure, guilt). The increased inward focus in depression is connected with a decreased environmental focus. The development of neuropsychodynamic hypotheses of the altered self-reference is based on the investigation of the emotional-cognitive interaction in depressed patients. It may be hypothesized that the increased negative self-attributions—as typical characteristics of an increased self-focus in depression—may result from altered neuronal activity in subcortical-cortical midline structures in the brain, especially from hyperactivity in the cortical-subcortical midline regions and hypoactivity in the lateral regions. The increased resting state activity in depression is especially associated with an increased resting state activity in the default mode network (DMN) and a dysbalance between DMN and executive network (EN) activity. Possible therapeutic consequences of the neuropsychodynamic approach to depression involve the necessary emotional attunement in psychotherapy of depressed patients and the adequate timing of therapeutic interventions. The hypotheses which have been developed in the context of the neuropsychodynamic model of depression may be used for more specific psychotherapeutic interventions, aiming at specific mechanisms of compensation and defence, which are related to the increased resting state activity and the disturbed resting state-stimulus-interaction. [ABSTRACT FROM AUTHOR]

Increased amygdala reactivity might lead to negative bias during emotional processing that can be reversed by antidepressant drug treatment. However, little is known on how N-methyl- d-aspartate (NMDA) receptor antagonism with ketamine as a novel antidepressant drug target might modulate amygdala reactivity to emotional stimulation. Using functional magnetic resonance imaging (fMRI) and resting-state fMRI (rsfMRI), we assessed amygdalo-hippocampal reactivity at baseline and during pharmacological stimulation with ketamine (intravenous bolus of 0.12 mg/kg, followed by a continuous infusion of 0.25 mg/kg/h) in 23 healthy subjects that were presented with stimuli from the International Affective Picture System (IAPS). We found that ketamine reduced neural reactivity in the bilateral amygdalo-hippocampal complex during emotional stimulation. Reduced amygdala reactivity to negative pictures was correlated to resting-state connectivity to the pregenual anterior cingulate cortex. Interestingly, subjects experienced intensity of psychedelic alterations of consciousness during ketamine infusion predicted the reduction in neural responsivity to negative but not to positive or neutral stimuli. Our findings suggest that the pharmacological modulation of glutamate-responsive cerebral circuits, which is associated with a shift in emotional bias and a reduction of amygdalo-hippocampal reactivity to emotional stimuli, represents an early biomechanism to restore parts of the disrupted neurobehavioral homeostasis in MDD patients. Hum Brain Mapp 37:1941-1952, 2016. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Depression and early life adversity (ELA) are associated with aberrant resting state functional connectivity (FC) of the default mode (DMN), salience (SN), and central executive networks (CEN). However, the specific and differential associations of depression and ELA with FC of these networks remain unclear. Applying a dimensional approach, here we analyzed associations of FC between major nodes of the DMN, SN, and CEN with severity of depressive symptoms and ELA defined as childhood abuse and neglect in a sample of 83 healthy and depressed subjects. Depressive symptoms were linked to increased FC within the SN and decreased FC of the SN with the DMN and CEN. Childhood abuse was associated with increased FC within the SN, whereas childhood neglect was associated with decreased FC within the SN and increased FC between the SN and the DMN. Our study thus provides evidence for differential associations of depressive symptoms and ELA with resting state FC and contributes to a clarification of previously contradictory findings. Specific FC abnormalities may underlie specific cognitive and emotional impairments. Future research should link specific clinical symptoms resulting from ELA to FC patterns thereby characterizing depression subtypes with specific neurobiological signatures. [ABSTRACT FROM AUTHOR]

Background: The higher prevalence of major depressive disorder (MDD) in females relative to males is well-established. Some authors have posited this difference arises to divergent symptom profiles in females vs. males. However, empirical tests of this hypothesis have yielded equivocal results. Here, we investigate sex differences in MDD of individual symptoms and symptom networks in a treatment-seeking sample.Methods: We assessed depressive symptoms using Hamilton Depression Rating Scale (HDRS-17) in 590 treatment-seeking adults with MDD (300 females). We examined group differences in symptom endorsement. We investigated symptom networks and estimated Gaussian Graphical Models. Finally, we compared the female and male networks using the Network Comparison Test.Results: Females scored significantly higher in psychological anxiety (p <0.001; rB = -0.155), somatic anxiety (p = .001; rB = -0.150) and feelings of guilt (p = .002; rB = -0.139). Male and female patients did not differ in depression sum scores. There were no sex differences in network structure or global strength.Limitations: Our study was sufficiently powered to detect only medium sized symptom differences. The generalizability of our study is limited to clinical samples and further studies are needed to investigate if findings also translate to outpatient samples.Conclusion: Females reported elevated anxiety symptoms and guilt. Clinicians should assess these symptom differences and tailor treatment to individual symptom profiles. No differences between sexes emerged in MDD network structures, indicating that features may be more similar than previously assumed. Sex differences in psychopathological features of MDD are important for future research and personalized treatment. [ABSTRACT FROM AUTHOR]