BACKGROUND
Schizophrenia is increasingly conceptualized as a disorder of large-scale brain network organization arising from atypical neurodevelopment. However, the relationship between early-emerging cortical folding patterns and the maturation of the structural connectome remains poorly understood.
METHODS
We introduced a sulcal morphology-centered framework that integrated normative modeling of sulcal width with diffusion-derived structural connectivity and cortical transcriptomics in a large multisite cohort (n=5,392; 377 schizophrenia). Deviations from normative folding patterns were mapped to the structural connectome and the Allen Human Brain Atlas.
RESULTS
Individuals with schizophrenia exhibited widespread sulcal widening (30/40 sulci), primarily in frontal, temporal, and occipital regions. Nodal vulnerability followed a clear topological principle: sulci with higher degree centrality (sulcal network hubs) showed disproportionately greater widening (pspin=0.02). Transcriptomic integration identified a gene expression profile explaining 56.5% of the spatial variance in sulcal abnormalities (p =0.049). This profile was significantly enriched for synaptic signaling and energy metabolism genes, showed adult-onset expression bias, and was associated with common cross-disorder genetic risk. Conversely, genes with the opposite spatial weight showed significant prenatal expression bias and enrichment for rare disruptive variants associated with autism spectrum disorder.
CONCLUSIONS
These findings demonstrate that aberrant cortical folding in schizophrenia is constrained by network topology and molecular architecture. By linking macroscopic folding to metabolic and synaptic pathways, this work establishes sulcal morphology as a mechanistically grounded biomarker that may help differentiate the neurodevelopmental trajectories of psychiatric disorders.
J. González-Peñas, H. Schnack, Carmen Rueda Hernández et al.· Biological Psychiatry· 0 citations
Abstract Background and Hypothesis Sleep disturbance is a well-established risk factor for suicide, though few studies to date have examined whether sleep disturbance contributes to suicide risk among individuals at clinical high risk for psychosis (CHR). The current study addressed this gap in the literature. We hypothesized that sleep disturbance would have a unique relationship with suicidal ideation/attempts when accounting for other variables in the model. We also hypothesized that the interaction between sleep disturbance/attenuated positive symptoms and sleep disturbance/stress would be related to suicidal ideation/attempts in CHR. Study Design The current study used data generated by the Accelerating Medicines Partnership® Schizophrenia Observational Study. The total sample included 1,048 participants (827 CHR and 221 community controls). Participants completed measures of suicidal ideation/attempts, attenuated positive symptoms, depressive symptoms, perceived stress, and sleep disturbance. Study Results Results supported a relationship between sleep disturbance and suicidal ideation/attempts in CHR, with participants who had lifetime ideation and attempts experiencing more sleep disturbance than those with no ideation or attempts. We also found small, but significant positive correlations between sleep disturbance and suicide risk in CHR. When accounting for other variables in the model, the effect of sleep disturbance remained significant for past month ideation, but not lifetime ideation or attempts. Both interaction models were non-significant. Conclusions Our findings highlight the potential value of sleep measures in early identification and treatment of suicide risk in CHR. Further research in this area is warranted.
H. Wastler, Aubrey M. Moe, Alexandra M Blouin et al.· Schizophrenia Bulletin Open· 0 citations
Prolonged CAL is linked to higher risk of FEP, preferentially affective psychosis in females, poorer functioning, and developmental potentiation of polygenic liability.
Á. Andreu-Bernabeu, J. González-Peñas, M. Bernardo et al.· Schizophrenia bulletin· 0 citations
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