The main goal of the study was to examine the relationship between anxiety and depressive symptoms and the perception of disinformation in the Czech population. The research was performed on a sample of 2867 respondents. Analytical processing was carried out through quasi-Poisson regression analysis separately for the three age groups (aged 16-39, 40-64, and 65-90). The dependent variables were the GAD-7 (Generalised Anxiety Disorder) and PHQ-9 (Patient Health Questionnaire) total scores, measuring anxiety and depressive symptoms, respectively. The independent variables were represented by the subjective perception of exposure, severity of disinformation, and credibility of specific disinformation in the Czech Republic. The 11 narratives, verified by a fact-checking organisation, were examined, of which eight were disinformation claims and three were factual reports. The outcomes demonstrated that 69.3% of the population experienced no or minimal anxiety, 19.0% mild, 7.2% moderate, and 4.5% severe anxiety. In the case of depression, 43.0% of the population demonstrated minimal symptoms, 25.4% mild, 9.9% moderate, and 14.3% no symptoms. After Benjamini-Hochberg false-discovery-rate (FDR) adjustment, perceived exposure to disinformation remained positively associated with GAD-7 and PHQ-9 scores across all three age groups. Among the 66 narrative-specific tests, 20 of 33 GAD-7 associations and 17 of 33 PHQ-9 associations remained statistically significant after FDR correction. The retained associations varied by narrative and age group rather than indicating a uniform age gradient. Because the data are cross-sectional, these associations do not establish causal direction.

Panic disorder is highly debilitating and contributes a significant amount to anxiety-related disability-adjusted life years globally. To understand this burden, the current study provides an up-to-date understanding of the descriptive epidemiology of panic attacks and panic disorder in the Australian population. Data were from the most recent 2020-2022 National Survey of Mental Health and Wellbeing, a large-scale population-based study conducted in Australian households with respondents aged 16-85 years of age (n = 15,893). Panic attacks and panic disorder experienced across the lifetime, within the past 12 months and within the past 30-days were assessed by the Composite International Diagnostic Interview according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) diagnostic criteria to facilitate direct comparisons with the 2007 National Survey of Mental Health and Wellbeing (n = 8841). The lifetime prevalence of panic attacks and panic disorder was ~27% and 4%, respectively. Those with panic disorder indicate a median age of onset in their early 20s and the experience of panic disorder is not trivial, with nearly half of all cases (45%) falling within the 'severe' range in terms of severity and functional impairment. There were significantly elevated odds in select subgroups of the population with evidence that panic attacks and panic disorder remain a pressing concern for the Australian population, and particularly so in 2020-22 for younger cohorts (16-24), females, those who have never been married, and people who reside in inner regional areas. Despite improvements in access to mental health services, there remains a strong need for improved mental health services and targeted prevention programmes.

Cyber victimization is among the most consistent predictors of depression (DEP) in adolescence, yet research has largely treated both constructs as unidimensional totals, obscuring which specific victimization experiences activate which depressive symptoms and for whom. This study applied a person-centered and network psychometric approach to map these pathways in a cross-sectional community sample of 622 Turkish adolescents (55.0% female; M aɡe = 13.90 years). Latent profile analysis (LPA) identified three distinct subgroups based on self-esteem (SE), family affluence, and social media (SM) use: a low SE/moderate SM group (n = 395, 63.5%), a high SE/high DEP group (n = 115, 18.5%), and a high SM use group (n = 112, 18.0%). Depressive symptom networks differed significantly in global strength across profiles; the high SM use group showed the densest intersymptom connections. A bipartite bridge network analysis revealed that self-harm/suicidal ideation was the strongest cross-community bridge node (bridge expected influence = 0.143), despite being the most peripheral symptom within the DEP network itself. This dissociation suggests that the symptom is linked mainly to cyber victimization rather than to other depressive symptoms. Embarrassing messages was the strongest victimization-side bridge node (EI = 0.095). These findings challenge the assumption that intranetwork centrality predicts intervention priority: Peripheral symptoms may function as critical entry points when external stressors drive activation.

This pre-registered systematic review and meta-analysis (PROSPERO CRD42023490547) evaluated the effectiveness of long-term psychodynamic psychotherapy (LTPP) in reducing depressive symptoms using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) framework and updated empirically supported treatment (EST) criteria. MEDLINE, PsycINFO, Embase, and the Cochrane Central Register of Controlled Trials were searched through January 16, 2025. Sixteen randomized controlled trials involving 1992 participants met inclusion criteria (LTPP ≥9 months, ≥30 sessions), encompassing varied populations, psychodynamic modalities, and comparator conditions. Effects were pooled using two- or three-level random-effects models. Risk of bias was assessed using Cochrane RoB 2. At treatment completion, LTPP showed significant reductions in depressive symptoms compared to all comparators (SMD = 0.34, 95% CI [0.20, 0.47]) and to active treatments specifically (SMD = 0.27, 95% CI [0.1, 0.45]). Effects were generally sustained at follow-up. Subgroup analyses revealed larger effects when LTPP was compared to active controls (SMD = 0.61), but with greater heterogeneity and very low certainty of evidence. GRADE assessments indicated high-certainty evidence for depressive symptom outcomes in the all-trials condition and moderate-certainty evidence in comparisons with active treatments. According to updated EST criteria, these findings support a Strong recommendation for LTPP in reducing depressive symptoms. However, limited evidence on functional outcomes, economic impact, and long-term maintenance precluded a Very Strong recommendation. Evidence from comparisons with active controls was of very-low certainty, supporting only a Weak recommendation. Risk of bias was a concern in most studies. Moderator analyses were prevented by small study numbers. Future individual patient data meta-analyses are needed to identify predictors of treatment response and to establish which subgroups of patients with depression are most suitable candidates for LTPP. Funding: Royal Australian and New Zealand College of Psychiatrists.

Depression has emerged as a globally prevalent mental disorder that severely compromises both physiological and psychological well-being. Its widespread prevalence constitutes a pressing public health concern that necessitates intensified attention and targeted therapeutic interventions. Clinical studies primarily delineate core symptomatology of depression and validate the therapeutic efficacy of candidate antidepressants in clinical cohorts. Complementarily, preclinical animal studies, predominantly utilizing chronic stress-induced rodent models, decipher the sophisticated molecular underpinnings of depression, and enable primary screening for high-potency antidepressants and innovative therapeutic regimens. Decades of clinical and preclinical research have substantially facilitated the establishment of diverse pathogenic hypotheses and development of first-line antidepressant therapies. To date, prevailing mechanistic hypotheses include classic theories regarding hypothalamic-pituitary-adrenal (HPA) axis dysregulation and monoamine deficiency, intermediate mechanisms centered on glutamate excitotoxicity and brain-derived neurotrophic factor dysregulation (BDNF), and emerging theories of neuroinflammation, oxidative stress, and microbiota-gut-brain (MGB) axis dysfunction. Currently available antidepressant regimens primarily comprise conventional monoamine-targeted agents and novel glutamate-modulating drugs (e.g., tricyclic antidepressants [TCAs], monoamine oxidase inhibitors [MAOIs], selective serotonin reuptake inhibitors [SSRIs], and esketamine), which, however, are plagued by inherent limitations and undesirable adverse reactions. Despite substantial advances achieved to date, further in-depth mechanistic investigations are still warranted to develop novel, safe, and efficacious antidepressants and optimize current therapeutic regimens. This review systematically recapitulates the prevailing pathogenic hypotheses and dissects associated multifaceted neurobiological underpinnings, with key evidence predominantly obtained from preclinical chronic stress rodent models. We outline the defining features of each mainstream hypothesis, and the intricate crosstalk and bidirectional regulatory networks among distinct mechanistic pathways, with a particular focus on underlying molecular signaling cascades, thereby constructing a holistic landscape of depression pathogenesis.