Mónica Flores-Ramos

Antenatal anxiety and depression frequently co-occur, negatively affecting maternal and offspring outcomes, yet their biological correlates remain insufficiently characterized. This cross-sectional study examined associations between anxiety and depressive symptoms and serum concentrations of brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and epidermal growth factor (EGF), proteins implicated in pregnancy-related vascular adaptations whose dysregulation has been associated with placental dysfunction and negative perinatal outcomes. A total of 148 women with uncomplicated second- and third-trimester pregnancies were assessed using the Hamilton Anxiety Rating Scale and Hamilton Depression Rating Scale. Serum BDNF levels were quantified by enzyme-linked immunosorbent assay, whereas VEGF and EGF were measured using a multiplex bead-based immunoassay during late pregnancy. Based on scale scores, participants were classified as controls, women with anxiety without depressive symptoms, or women with anxiety and depressive symptoms. In the between-group comparisons, women with clinically significant anxiety exhibited higher BDNF and EGF levels than controls. Regression analyses indicated that anxiety severity was positively associated with BDNF, VEGF, and EGF levels (all p < 0.05), whereas depressive symptom severity was negatively associated with BDNF levels (p < 0.05). These findings suggest distinct associations of antenatal anxiety and depressive symptoms with circulating growth factors, particularly BDNF, and warrant further investigation of vascular–immune–neurotrophic pathways potentially involved in perinatal mental health.

Antenatal anxiety and depression are common and frequently comorbid, affecting maternal and offspring outcomes; however, their underlying biological correlates remain incompletely understood. This cross-sectional study examined whether peripheral levels of brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and epidermal growth factor (EGF) were associated with anxiety and depressive symptoms during late pregnancy. A total of 148 women with uncomplicated second and third-trimester pregnancies was assessed using the Hamilton Anxiety Rating Scale and Hamilton Depression Rating Scale. Serum BDNF levels were quantified by ELISA, whereas VEGF and EGF were measured using a multiplex bead-based immunoassay. Based on scale scores, participants were classified as controls, women with anxiety without depressive symptoms, or women with anxiety and depressive symptoms. In the between-group comparisons, women with clinically significant anxiety exhibited higher BDNF and EGF levels than controls, whereas differences in VEGF levels did not reach statistical significance. Regression analyses indicated that anxiety severity was positively associated with BDNF, VEGF, and EGF levels, whereas depressive symptom severity was negatively associated with BDNF levels. These findings suggest distinct associations of antenatal anxiety and depressive symptoms with circulating growth factors, particularly BDNF, and warrant further investigation of vascular–immune–neurotrophic pathways potentially involved in perinatal mental health.

Major depressive disorder (MDD) is among the most common and disabling psychiatric disorders. MDD is multifactorial, influencing the central nervous, endocrine, and immune systems. Also, MDD impacts neurochemical and inflammatory pathways via shared signaling mechanisms, including metabolites, soluble factors, and extracellular vesicles (EVs, including exosomes). Here, we hypothesized that EVs from MDD patients or mice exposed to chronic unpredictable mild stress (CUMS) contain specific inflammatory signatures that may help explain the pathophysiology of that mental disorder. We included four groups: healthy female controls (n = 8), women with MDD (n = 12), healthy Balb/C female mice (n = 10), and Balb/C mice under CUMS (n = 10). We isolated and characterized exosome-enriched EVs from human and murine serum and analyzed their protein content using antibody arrays. We identified three protein sets with significant differences (p < 0.05): 36 human exosome proteins decreased in the MDD group; 18 murine exosome proteins decreased in the CUMS group; and 12 proteins showed differential expression between human and murine exosomes, mostly trending downward in the CUMS and MDD groups. We performed bioinformatic analysis to determine protein–protein interactions and gene ontology functions. We identified signaling pathways associated with MDD and chronic stress: chemokine, cytokine–cytokine receptor, JAK-STAT, pathways in cancer, Rap1, Ras, TNF signaling, and cytokine interactions. These findings highlight the importance of human and murine exosomes as critical sources for understanding depression’s molecular mechanisms.

Introduction. Schizoaffective disorder is a complex condition whose clinical manifestations overlap with those of schizophrenia, bipolar disorder, and depression. It is notoriously difficult to diagnose using the DSM-5 and ICD-11. Both the similarities with other diagnoses and the differences between the guidelines of these two diagnostic symptoms hamper its accurate diagnosis. Magnetic resonance imaging, however, is designed to identify specific differences and similarities in brain structures between disorders. Objective. To compare the total intracranial volume, gray matter, white matter, and cerebrospinal fluid in subjects with a schizophrenia or schizoaffective disorder diagnosis using a magnetic resonance imaging database drawn up by the INPRFM. Method. The images of 55 subjects per group (schizophrenia and schizoaffective disorder) were analyzed. The volumetric study was conducted using the CAT12 program for each of the images to obtain the total intracranial volume. The volumes of gray matter, white matter, cerebrospinal fluid, and total volume were compared using a general linear model including sex and group as fixed factors. Results. White matter volume was lower in schizophrenia, with no differences being observed by sex or sex and group interaction. No differences were found between groups in the remaining measurements. Discussion and conclusion. The study provides evidence of general neuroanatomical differences in schizoaffective disorder, supporting the notion that it is not just a variant of schizophrenia, but a clinically and biologically distinct condition.

Background: Despite the well-documented benefits of environmental enrichment (EE) in animal models of depression, the application of these findings to humans is complex due to individual variability and environmental constraints. Aim: This study aims to investigate the relationship between EE and depression by comparing demographic features and EE levels between individuals with depression and controls. Methods: A cross-sectional, comparative retrospective study was conducted in a specialized psychiatric facility in Mexico City. Ninety-six control subjects and 86 individuals with major depression (MD) were recruited. Participants with MD were diagnosed according to DSM-5 criteria and scored a minimum of 13 on the 17-item Hamilton Depression Rating Scale (HDRS). Demographic information and EE were assessed using the Environmental Enrichment indicator (EEI), which includes cognitive, social, and physical activity dimensions. Statistical analyses included chi-square tests, t -tests, and logistic regression to identify associations between demographic variables, EE, and depression. Results: The findings indicated that individuals with MD had lower EE levels compared to controls. Significant predictors of depression included low EE, being unemployed or a housewife, and female gender, while higher education decreased depression risk. Low EE mediated the relationship between occupation and depression. Additionally, the impact of demographic factors on depression was also strongly influenced by the levels of EE. Conclusion: Socio-demographic characteristics, such as female gender and occupation were associated with depression; additionally, a low level of EE was a predictor of depression. A higher education diminished the depression risk.

Background: Major depressive disorder (MDD) is a prevalent neuropsychiatric condition associated with significant functional impairment and reduced quality of life. Environmental enrichment (EE), a model encompassing cognitive, social, and physical activities, has demonstrated antidepressant effects in animal models through mechanisms involving brain plasticity. In humans, the influence of EE on depressive symptoms and its clinical significance remain under investigation. This study evaluated the relationship between EE domains and the clinical symptoms of MDD, focusing on the possible modulatory effects of EE on depressive symptomatology. Methods: We conducted an observational, cross-sectional study involving 50 adults diagnosed with MDD. Depressive symptoms were assessed using the 17-items Hamilton Depression Rating Scale (17-HDRS), and EE levels were measured using the Environmental Enrichment Indicator (EEI), which evaluates cognitive, social, and physical activity domains. Correlations between depressive symptoms and EEI domains were analyzed. Results: Participants with higher 17-HDRS scores generally exhibited lower levels of EE. Additionally, individuals with more severe depressive symptoms were less likely to engage in cognitive activities compared to those with milder symptoms; however, this difference was not statistically significant (Kruskal–Wallis test, H = 3.82, df = 2, p = 0.14). Notably, higher EE levels were observed among younger participants. Conclusions: The level of EE in individuals with depression may affect symptom severity. Further studies in clinical populations are needed to clarify the relationship between EE and depressive symptoms.

Maternal behavior encompasses a range of biologically driven responses whose expression and duration vary across species. Maternal responses rely on robust adaptive changes in the female brain, enabling mothers to engage in caregiving, nourishing, and offspring protection. Morphological and functional changes in the maternal brain enhance sensitivity to offspring cues, eliciting maternal behaviors, rewarding responses, and social processing stimuli essential for parenting. Maternal behavior comprises a range of biological responses that extend beyond basic actions, reflecting a complex, evolutionarily shaped neurobiological adaptation. These behaviors can be broadly categorized into direct behaviors, which are explicitly aimed at the care of the offspring, and indirect behaviors that, overall, ensure the protection, nourishment, and survival of the newborn. The secretion of main neuropeptide hormones, such as oxytocin (OT), prolactin (PRL), and placental lactogens (PLs), during the peripartum period, is relevant for inducing and regulating maternal responses to offspring cues, including suckling behavior. Although PRL is primarily associated with reproductive and parental functions in vertebrates, it also modulates distinct neural functions during pregnancy that extend from lactogenesis to adult neurogenesis, neuroprotection, and neuroplasticity, all of which contribute to preparing the maternal brain for motherhood and parenting interactions. Parvocellular OT-containing neurons in the paraventricular nucleus (PVN) and in the anterior hypothalamic nucleus (AHN) project axon collaterals to the medial preoptic area, which, in turn, projects to the nucleus accumbens (NACC) and lateral habenula (lHb) via the retrorubral field (RRF) and the ventral tegmental area (VTA), which mediate the motivational aspects of maternal responses to offspring cues. The reshaping process of the brain and neural networks implicated in motherhood depends on several factors, such as up- and downregulation of neuronal gene expression of bioactive peptide hormones (i.e., OT, PRL, TIP-39, galanin, spexin, pituitary adenylate cyclase-activating polypeptide (PACAP), corticotropin-releasing hormone (CRH), peptide receptors, and transcription factors (i.e., c-fos and pSTAT)) in target neurons in hypothalamic nuclei, mesolimbic areas, the hippocampus, and the brainstem, which, overall, regulate the expression of maternal behavior to offspring cues, as shown in postpartum female rodents. In this review, we describe the modulatory neuropeptides, the neural networks underlying peptide transmission systems, and cell signaling involved in parenthood. We highlight the dysregulation of neuropeptide hormones and their receptors in the central nervous system in relation to psychiatric disorders.

Background: Adipokines secreted by the adipose tissue and placenta play a critical role in regulating metabolic functions that are essential for fetoplacental development and embryonic growth. While adipokines are known to impact a wide range of physiological and pathological conditions, their role in affective disorders during pregnancy remains underexplored. In this study, we aimed to assess the serum levels of distinct adipokines and examine their association with anxiety and comorbid depression in pregnant women. Methods: Third-trimester pregnant women with severe anxiety (ANX, n = 45) and anxiety plus depressive symptoms (ANX + DEP, n = 61) were enrolled in the study, along with healthy control subjects (CTRL, n = 33). Participants were classified using the Hamilton Anxiety Rating Scale (HARS) and the Hamilton Depression Rating Scale (HDRS). Serum levels of adiponectin, adipsin, leptin, and resistin were quantified by flow cytometry-based immunoassay. Clinical, biochemical, and demographic parameters were analyzed using ANOVA with a post hoc Tukey test. Pearson bivariate and partial correlations were performed to assess associations between variables. Results: Adipokine serum levels were significantly higher in the symptomatic groups (ANX, ANX + DEP) than in the CTRL group (p < 0.001). Adiponectin, leptin, and resistin levels positively correlated with anxiety symptoms (HARS, p < 0.01). Furthermore, resistin levels showed a strong association with depressive symptoms (HDRS, p = 0.001) in the ANX + DEP group, after adjusting all parameters by clinical confounders. Conclusions: Our findings revealed that both pro- and anti-inflammatory adipokine levels are elevated in women with affective symptoms during late pregnancy. Pro-inflammatory properties of leptin and resistin may contribute to the severity of anxiety symptoms. Notably, resistin emerges as a key adipokine associated with the expression of depressive symptoms. In addition, adiponectin, acting as an anti-inflammatory mediator, may counteract the inflammatory responses induced by leptin and resistin. These results provide new insights into the role of specific adipocytokine in women with affective disorders during late pregnancy.