Journal of affective disorders最新文献

Objective: To examine the efficacy of intermittent theta burst stimulation (iTBS) for depressive symptoms and anhedonia in adolescents with depression, and explore potential moderators of treatment response.

Methods: We conducted a randomized controlled trial enrolling 60 adolescents (11-19 years) with depression from a tertiary hospital in Anhui Province, China; with participant-and assessor-blinding, whereas TMS operators were not. Participants were allocated by an independent researcher using a computer-generated random number list to active iTBS (n = 30) or sham stimulation (n = 30). The intervention was delivered over two weeks (10 treatment days), with three sessions per weekday(30 sessions total). Clinical assessments were performed at baseline and post-intervention using standardized instruments: the Hamilton Depression Rating Scale-17 items (HAMD-17), Hamilton Anxiety Rating Scale-14 items (HAMA-14), and Temporal Experience of Pleasure Scale (TEPS). Treatment effects were examined using 2 × 2 repeated-measures ANOVA, and exploratory moderation was examined using PROCESS Model 1 with 5000 bootstrap resamples, with Holm-Bonferroni correction applied across five interaction tests.

Results: Baseline clinical scale scores were comparable between groups (P > 0.05). Following treatment, significant group× time interactions indicated greater improvement in the active iTBS group than sham on depressive symptoms (HAMD-17: F = 40.300, P < 0.001) and anxiety symptoms (HAMA-14: F = 23.802, P < 0.001). Significant group× time interactions were also observed for TEPS total and its four subscales (P < 0.05). In exploratory moderation analyses, the Group×baseline TEPS-AA interaction was nominally significant(P = 0.014) but did not survive Holm-Bonferroni correction(adjusted P = 0.070).

Conclusion: iTBS was feasible and associated with greater short-term improvements in depressive symptoms and anhedonia in adolescents compared with sham stimulation. Exploratory analyses indicated that baseline hedonic traits (particularly abstract anticipatory pleasure) may be related to differential treatment response, but moderation effects should be interpreted cautiously given multiple-testing correction and require confirmation in adequately powered trials with longer follow-up. These findings support further investigation of iTBS for adolescent depression and the prospective evaluation of candidate predictors of response. Generalizability may be limited by the single-center design and the accelerated treatment schedule.

Background: Prolonged Grief Disorder (PGD) in later life may involve volumetric patterns indicative of accelerated brain aging. This study examined whether structural brain age differs between individuals with PGD and those with integrated grief (IG), and whether it is associated with clinical severity.

Methods: Chronically grieving older adults with PGD (n = 36) and IG (n = 56), equated on demographics and time since loss, underwent structural MRI. Machine learning-derived indices were computed for each participant: Brain Age Gap (SPARE-BAG), Alzheimer's disease-like atrophy (SPARE-AD), and five dominant brain aging patterns. Group differences and associations with symptom severity were assessed, along with moderation by age, cognitive status, medical burden, and current and past depression.

Results: Compared to IG, the PGD group showed significantly higher SPARE-BAG (t = 2.61, p_corrected = 0.021), SPARE-AD (t = 2.04, p_corrected = 0.045), and medial temporal lobe atrophy pattern (t = 3.44, p_corrected = 0.005). However, these findings were attenuated and no longer significant after accounting for comorbid depressive symptoms. In the PGD group, both SPARE scores positively correlated with grief and depressive symptom severity (p_corrected < 0.03). The SPARE-BAG-grief symptom association was moderated by younger age (z = -2.92, p_FDR = 0.018) and higher depressive symptoms (z = 1.88, p = 0.061); SPARE-AD-depressive symptom correlation was moderated by past depression history (z = 2.64, p_corrected = 0.041).

Conclusion: Adults with PGD exhibit structural brain patterns consistent with accelerated and AD-like aging. However, these findings were largely driven by comorbid depressive symptoms. The brain aging indices were associated with both grief and depressive symptom severity, highlighting the cumulative neurobiological burden associated with PGD and co-occurring depression and underscoring the need for integrative clinical approaches addressing both conditions.

Introduction: Suicide is a leading cause of premature death, with risk peaking around psychiatric hospitalization. Emotion dysregulation (ED) is recognized as a key factor contributing to suicidal ideation and behavior across psychiatric diagnoses. The efficacy of interventions that target ED for suicidality reduction remains unclear, so we aimed to assess these interventions in psychiatric inpatients.

Methods: We conducted a PRISMA-compliant, PROSPERO-registered (CRD420251140949) systematic review and meta-analysis of randomized and non-randomized trials evaluating interventions targeting emotion regulation (ER) for psychiatric inpatients with suicidal ideation and/or behavior. Searches covered PubMed, Embase, and PsycINFO to September 18, 2025. Standardized mean differences (Hedges' g) were pooled under random-effects models and heterogeneity was assessed (Q, I², τ²). Exploratory meta-regressions examined age, sex, and study quality; small-study effects were explored with funnel plots.

Results: Twelve studies met inclusion (n = 1708), spanning dialectical behavior therapy (DBT), mindfulness-based interventions, acceptance and commitment therapy (ACT), and other ER-related protocols. Across modalities, feasibility and acceptability were high and interventions consistently improved suicide-related outcomes in transdiagnostic adolescents and adult populations. Suicide attempts and ideation met outcome criteria for exploratory meta-analyses, and, for both, ER-targeted interventions outperformed usual care, despite heterogeneity and small samples. Exploratory meta-regressions were non-significant; funnel plots did not suggest marked publication bias, though power was limited.

Conclusions: ER-targeted interventions delivered during psychiatric hospitalization are feasible and show promising benefits on suicide-related outcomes. Given heterogeneity and limited sample sizes, larger, well-powered randomized trials using standardized suicidality endpoints are needed to establish efficacy, refine inpatient protocols, and inform acute care pathways.

Speech encodes emotional, cognitive, and motor states, offering an objective, non-invasive window into mental health. In major depressive disorder (MDD), vocal alterations are reported, yet their cross-dataset reproducibility, symptom specificity, and longitudinal stability remain uncertain, especially under naturalistic, content-variable speech tasks. We conducted a large, multi-cohort study of 1857 participants spanning a primary discovery dataset, an independent secondary clinical dataset, and an 8-week longitudinal follow-up. From standardized recordings we extracted 6373 acoustic features and examined (i) baseline case-control screening in each dataset, (ii) severity-related feature patterns across depression levels, (iii) symptom-dimension markers using stability-enhanced elastic net, and (iv) longitudinal feature changes over 8 weeks, integrating unsupervised clustering and mediation analyses, with false discovery rate control. Across cohorts, correlation-based redundancy reduction yielded a compact final set of 23 non-redundant representative features for cross-cohort reporting and interpretation. Symptom-factor analysis identified distinct, non-overlapping feature sets for HAMD-24 dimensions, with somatic and depressed mood yielding the most stable markers. Longitudinally, 38 features exhibited heterogeneous recovery trajectories and mediation patterns consistent with symptom improvement, with spectral-shape and modulation markers showing higher temporal sensitivity than energy and voice-quality features. Overall, our findings indicate that a compact set of speech-derived markers can support symptom-informed monitoring in MDD. A small subset of acoustic features is robust, symptom-specific, and temporally informative, refining assumptions of uniform vocal change and enabling targeted, symptom-informed speech biomarkers for personalized monitoring and early intervention. Future work should verify these markers using task-matched speech prompts and alternative feature representations, given potential content-related confounding in free-response speech and reported reliability limitations of some high-dimensional acoustic feature toolkits. TRIAL REGISTRATION: ChiCTR2500095151.

Anxiety symptoms are highly prevalent in major depressive disorder (MDD) and significantly influence clinical outcomes, yet neurophysiological mechanisms underlying anxiety severity remain poorly understood. To characterize neurophysiological alterations associated with different levels of anxiety severity in drug-naïve MDD, we used resting-state electroencephalogram (EEG) microstate analysis. Resting-state EEG was recorded from 113 MDD patients with varying anxiety levels (DDA) and 60 healthy controls (HC). Patients were stratified into low (DDLA), moderate (DDMA), and severe (DDSA) groups using the Hamilton Anxiety Rating Scale. K-means clustering identified seven microstate classes (A-G). Microstate B duration was reduced in all patient groups compared with HC, indicating visual network dysfunction common to depression. Microstate G-corresponding to sensorimotor and interoceptive networks-showed robust progressive alterations, with duration, occurrence, and coverage increasing from DDLA to DDMA and DDSA. Non-random transition pairs were reduced in patients compared with HC (22 pairs) but increased progressively with anxiety severity (DDLA: 10, DDMA: 16, DDSA: 18 pairs). The degree of anxiety was positively correlated with significantly enhanced transitions between microstates D, F, and G (executive control, anterior default mode network, and sensorimotor networks). Microstate G parameters and anxiety severity were found to be positively correlated in the DDA patient. Microstate G may index anxiety severity at the neurophysiological level in depressed patients with anxiety, and progressive D-F-G network disruption reflects cumulative dysregulation of large-scale brain networks associated with co-occurring anxiety. These findings may have implications for biomarker development and targeted interventions.

Background: Anhedonia-a core symptom of mood disorders-reflects impairments in both reward anticipation and reward consumption. While its neurobiological underpinnings have been extensively studied in adults, considerably less is known about adolescent populations, despite critical neurodevelopmental changes during this period. This scoping review aims to map current evidence onto neurobiological correlates of anhedonia in adolescents with mood disorders.

Methods: A systematic search was conducted in PubMed and PsycInfo to identify studies investigating anhedonia in adolescents with mood disorders using neuroimaging techniques. Due to heterogeneity in study design and outcomes, findings were synthesized narratively.

Results: Twenty-one articles met the inclusion criteria, reporting on 1278 patients. The analysis revealed that anhedonia involves (1) increased frontal and decreased striatal activity during reward/incentive processing, and activation of regions of the limbic system during loss-related error processing; (2) striatal and corticolimbic activity during emotional processing; (3) reduced medial prefrontal cortex activity during cognitive processing; (4) involvement of corticostriatal and corticolimbic functional connectivity networks; (5) an inverse association between cerebral blood flow in corticolimbic and frontal regions in cerebral blood flow analysis; (6) altered alpha and theta activity and reduced cortical reactivity, and that; (7) GABA involvement in anhedonia remains inconclusive.

Conclusions: The neurobiological signatures of anhedonia in adolescents appear to involve altered activation and connectivity in reward-related circuits, particularly during anticipatory and error-processing phases. These findings underscore the need for greater methodological consistency, standardized phenotyping of anhedonia, and longitudinal studies to better understand developmental trajectories and inform early interventions.