Vazquezchan3691

Maternal mental health problems often develop prenatally and predict post-partum mental health. However, the circumstances before and following childbirth differ considerably. We currently lack an understanding of dynamic variation in the profiles of depressive and anxiety symptoms over the perinatal period.

Depressive and anxiety symptoms were self-reported by 980 women at 26-week pregnancy and 3 months post-partum. We used network analysis of depressive and anxiety symptoms to investigate if the symptoms network changed during and after pregnancy. The pre- and post-partum depressive-anxiety symptom networks were assessed for changes in structure, unique symptom-symptom interactions, central and bridging symptoms. We also assessed if central symptoms had stronger predictive effect on offspring's developmental outcomes outcomes at birth and 24, 54, and 72 months old than non-central symptoms. Bridging symptoms between negative and positive mental health were also assessed.

Though the depressive-anxiety on. Interventions and public health policies should thus be tailored to specific pre- and post-partum symptom profiles.

The differences between pre- and post-partum networks suggest that the presentation of maternal mental health problems varies over the peripartum period. This variation is not captured by traditional symptom scale scores. The bridging symptoms also suggest that anxiety symptoms may precede the development of maternal depression. Interventions and public health policies should thus be tailored to specific pre- and post-partum symptom profiles.The onset of puberty and related hormones exerts significant effects on brain morphometric and psychosocial development. The biological mechanisms underlying how the reactivation of the hypothalamic-pituitary-gonadal (HPG) axis and puberty-related hormonal maturation sculpts human brain architecture remain elusive. To address this question, 105 premature pubertal girls (age 8-11 years) without menstruation underwent brain structural scanning on a 3T MR system, and the luteinizing hormone releasing hormone (LHRH) stimulation test was used to identify the reactivation of the HPG axis. Among the 105 girls, 63 were positive for HPG axis reactivation (HPG+), while the others showed negative (HPG-). selleckchem Cortical thickness was calculated and compared between the two groups after adjusting for age. The brain regions showing inter-group differences were then extracted and correlated with the peak value of serum hormone after the LHRH stimulation test in entire sample. Compared to HPG- girls, HPG+ girls showed reduced cortical thickness mainly in the the right precuneus, right inferior temporal gyrus, and right superior frontal gyrus, while increased cortical thickness primarily in the left superior parietal lobe and right inferior parietal lobe. Linear-regression analysis revealed negative correlations between the cortical thickness of the right inferior parietal lobe with the peak value of FSH and the right precuneus with LH and E. These findings provide evidence to support the notion that the reactivation of HPG axis and changes of hormones during the early phase of hormonal maturation exert influences on the development of gray matter.Accumulating evidence suggests that childhood maltreatment (CM) confers risk for psychopathology later in life by inducing hypervigilance to social threat cues such as fearful faces. However, it remains unclear whether the modulatory impact of CM extents to the olfactory domain of social communication in humans. To address this question, we examined whether CM modulates the neural processing of chemosensory threat signals in sweat and whether CM affects the stress-reducing effects of oxytocin (OXT) in this context. In a randomized, double-blind within-subject functional MRI study design, 58 healthy participants (30 females) received intranasal OXT (40 IU) or placebo (PLC) and completed a forced-choice emotion recognition task with faces of varying emotion intensities (neutral to fearful) while exposed to sweat stimuli and a non-social control odor. Axillary sweat samples were collected from 30 healthy male donors undergoing an acute psychosocial stressor (stress) and ergometer training (sport) as control in aific effects of OXT in the olfactory domain are more pronounced in participants with increasing levels of CM exposure.According to the stress-diathesis model of suicidal behavior, completed suicide depends on the interaction between psychosocial stressors and a trait-like susceptibility. While there are likely multiple biological processes at play in suicidal behavior, recent findings point to over-activation of microglia, the resident macrophages of the central nervous system, as implicated in stress-induced suicidal behavior. However, it remains unclear how microglial dysregulation can be integrated into a clinical model of suicidal behavior. Therefore, this narrative review aims to (1) examine the findings from human post-mortem and neuroimaging studies that report a relationship between microglial activation and suicidal behavior, and (2) update the clinical model of suicidal behavior to integrate the role of microglia. A systematic search of SCOPUS, PubMed, PsycINFO, and Embase databases revealed evidence of morphological alterations in microglia and increased translocator protein density in the brains of individuals with suicidality, pointing to a positive relationship between microglial dysregulation and suicidal behavior. The studies also suggested several pathological mechanisms leading to suicidal behavior that may involve microglial dysregulation, namely (1) enhanced metabolism of tryptophan to quinolinic acid through the kynurenine pathway and associated serotonin depletion; (2) increased quinolinic acid leading to excessive N-methyl-D-aspartate-signaling, resulting in potential disruption of the blood brain barrier; (3) increased quinolinic acid resulting in higher neurotoxicity, and; (4) elevated interleukin 6 contributing to loss of inhibition of glutamatergic neurons, causing heightened glutamate release and excitotoxicity. Based on these pathways, we reconceptualized the stress-diathesis theory of suicidal behavior to incorporate the role of microglial activity.