Severe mental disorders (SMDs) impose profound suffering on patients and heavy burdens on family caregivers, often resulting in abusive behaviors. This study aimed to examine the association between psychiatric symptom severity and caregiver abuse, and to assess whether caregiver tobacco dependence moderates this relationship.

A cross-sectional study included 763 patient–caregiver dyads in rural Shandong, China. Psychiatric symptom severity was measured using the 18-item Brief Psychiatric Rating Scale. Caregiver tobacco dependence was assessed using the Fagerström Test for Nicotine Dependence. Patients reported caregivers’ verbal/physical abuse in the past year. Ordered logistic regression and interaction terms tested associations and moderation.

Overall, 25.7% of caregivers engaged in verbal abuse and 14.9% in physical abuse. Psychiatric symptom severity was significantly associated with both verbal (OR = 1.018, 95% CI: 1.010–1.026) and physical abuse (OR = 1.015, 95% CI: 1.005–1.025). Caregivers with moderate to severe tobacco dependence were more likely to commit verbal (OR = 1.851, 95% CI: 1.136–3.016) and physical abuse (OR = 2.292, 95% CI: 1.287–4.079) than non-smokers. Moderate to severe tobacco dependence significantly amplified the association between psychiatric symptom severity and verbal abuse (interaction OR = 1.024, 95% CI: 1.002–1.046), but not physical abuse.

In rural China, greater psychiatric symptom severity among patients with SMDs is associated with increased frequency of both verbal and physical abuse by caregivers, particularly verbal abuse among those with moderate to severe tobacco dependence, underscoring the need for caregiver-targeted psychological support and tobacco cessation interventions.

Schizophrenia progresses through high-risk, first-episode, and chronic stages, each associated with altered spontaneous brain activity. Resting state functional MRI studies highlight these changes, but inconsistencies persist, and the genetic basis remains unclear.

A neuroimaging meta-analysis was conducted to assess spontaneous brain activity alterations in each schizophrenia stage. The largest available genome-wide association study (GWAS) summary statistics for schizophrenia (N = 53,386 cases, 77,258 controls) were used, followed by Hi-C-coupled multimarker analysis of genomic annotation (H-MAGMA) to identify schizophrenia-associated genes. Transcriptome-neuroimaging association and gene prioritization analyses were performed to identify genes consistently linked to brain activity alterations. Biological relevance was explored by functional enrichment.

Fifty-two studies met the inclusion criteria, covering the high-risk (Nhigh-risk = 409, Ncontrol = 475), first-episode (Ncase = 1842, Ncontrol = 1735), and chronic (Ncase = 1242, Ncontrol = 1300) stages. High-risk stage showed reduced brain activity in the right median cingulate and paracingulate gyri. First-episode stage revealed increased activity in the right putamen and decreased activity in the left gyrus rectus and right postcentral gyrus. Chronic stage showed heightened activity in the right inferior frontal gyrus and reduced activity in the superior occipital gyrus and right postcentral gyrus. Across all stages, 199 genes were consistently linked to brain activity changes, involved in biological processes such as nervous system development, synaptic transmission, and synaptic plasticity.

Brain activity alterations across schizophrenia stages and genes consistently associated with these changes highlight their potential as universal biomarkers and therapeutic targets for schizophrenia.

Little is known regarding the shared genetic architecture underlying the phenotypic associations between depression and preterm birth (PTB). We aim to investigate the genetic overlap and causality of depression with PTB.

Leveraging summary statistics from the largest genome-wide association studies for broad depression (Ntotal = 807,533), major depression (Ntotal = 173,005), bipolar disorder (Ntotal = 414,466), and PTB (Ntotal = 226,330), we conducted a large-scale genome-wide cross-trait analysis to assess global and local genetic correlations, identify pleiotropic loci, and infer potential causal relationships

Positive genetic correlations were observed between PTB and broad depression (rg = 0.242), major depression (rg = 0.236), and bipolar disorder (rg = 0.133) using the linkage disequilibrium score regression, which were further verified by the genetic covariance analyzer. Local genetic correlation was identified at chromosome 11q22.3 (harbors NCAM1-TTC12-ANKK1-DRD2) for PTB with depression. Cross-trait meta-analysis identified two loci shared between PTB and broad depression, two loci shared with major depression, and five loci shared with bipolar disorder, among which three were novel (rs7813444, rs3132948 and rs9273363). Mendelian randomization demonstrated a significantly increased risk of PTB for genetic liability to broad depression (odds ratio [OR]=1.30; 95% confidence interval [CI]: 1.11-1.52) and major depression (OR=1.27; 95%CI: 1.08-1.49), and the estimates remained significant across the sensitivity analyses.

Our findings demonstrate an intrinsic link underlying depression and PTB and shed novel light on the biological mechanisms, highlighting an important role of early screening and effective intervention of depression in PTB prevention, and may provide novel treatment strategies for both diseases.