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Schizophrenia is a prototypical network disorder with widespread brain-morphological alterations, yet it remains unclear whether these distributed alterations robustly reflect the underlying network layout. We tested whether large-scale structural alterations in schizophrenia relate to normative structural and functional connectome architecture, and systematically evaluated robustness and generalizability of these network-level alterations. Leveraging anatomical MRI scans from 2439 adults with schizophrenia and 2867 healthy controls from 26 ENIGMA sites and normative data from the Human Connectome Project (n = 207), we evaluated structural alterations of schizophrenia against two network susceptibility models: (i) hub vulnerability, which examines associations between regional network centrality and magnitude of disease-related alterations; (ii) epicenter mapping, which identifies regions whose typical connectivity profile most closely resembles the disease-related morphological alterations. To assess generalizability and specificity, we contextualized the influence of site, disease stages, and individual clinical factors and compared network associations of schizophrenia with that found in affective disorders. Our findings show schizophrenia-related cortical thinning is spatially associated with functional and structural hubs, suggesting that highly interconnected regions are more vulnerable to morphological alterations. Predominantly temporo-paralimbic and frontal regions emerged as epicenters with connectivity profiles linked to schizophrenia's alteration patterns. Findings were robust across sites, disease stages, and related to individual symptoms. Moreover, transdiagnostic comparisons revealed overlapping epicenters in schizophrenia and bipolar, but not major depressive disorder, suggestive of a pathophysiological continuity within the schizophrenia-bipolar-spectrum. In sum, cortical alterations over the course of schizophrenia robustly follow brain network architecture, emphasizing marked hub susceptibility and temporo-frontal epicenters at both the level of the group and the individual. Subtle variations of epicenters across disease stages suggest interacting pathological processes, while associations with patient-specific symptoms support additional inter-individual variability of hub vulnerability and epicenters in schizophrenia. Our work outlines potential pathways to better understand macroscale structural alterations, and inter- individual variability in schizophrenia.
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http://dx.doi.org/10.1038/s41380-024-02442-7 | DOI Listing |
Biochem Biophys Res Commun
September 2025
Departamento de Ciencias Químico-Biológicas, Instituto de Ciencias Biomédicas, Universidad Autónoma de Ciudad Juárez, Ciudad Juárez, Mexico. Electronic address:
Chlorpromazine (CPZ) is a first-generation antipsychotic that has been widely used to treat an array of neurological conditions, including schizophrenia, bipolar disorder, and anxiety. Treatment of these chronic conditions with CPZ has been linked to elevated levels of reactive oxygen species (ROS), and accumulating evidence supports a link between ROS and chronic and degenerative pathologies, including cardiovascular diseases. Therefore, the aim of this study was to observe the presence of oxidative stress in porcine aortic endothelial cells (PAE) exposed to different concentrations of CPZ in vitro.
View Article and Find Full Text PDFSchizophr Res
September 2025
Department of Psychiatry, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX, 75390, USA. Electronic address:
Alterations in hippocampal structure and function are established in schizophrenia. However, the specific patterns of hippocampal activity along the schizophrenia course remain unknown. Eighty-five study participants [34 schizophrenia probands (SZ), 32 first-degree relatives (REL), 19 healthy controls (HC)] underwent 3Tesla ultra-high resolution brain MRI (Vascular Space Occupancy); relative cerebral blood volume (rCBV)-an index of regional activity-was estimated across hippocampal subfields: dentate gyrus (DG), CA3, CA1, and subiculum (SUB).
View Article and Find Full Text PDFMol Psychiatry
September 2025
Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, 16 De Crespigny Park, London, SE5 8AB, UK.
Disrupted gamma-aminobutyric acid (GABA) neurotransmission may contribute to the pathophysiology of schizophrenia. Reductions in hippocampal GABAergic neurons have been found in schizophrenia, and increased hippocampal perfusion has been described in schizophrenia and in people at clinical high-risk for psychosis (CHRp). We have also found decreases in hippocampal GABA receptors containing the α5 subunit (GABARα5) in a well-validated neurodevelopmental rat model of relevance for schizophrenia.
View Article and Find Full Text PDFJ Affect Disord
September 2025
Tianjin University, Medical School, Tianjin, China; Tianjin University, Haihe Laboratory of Brain-Computer Interaction and Human-Machine Integration, Tianjin, China; Tianjin University, State Key Laboratory of Advanced Medical Materials and Medical Devices, Tianjin, China.
Background: Abnormal gamma-band auditory steady-state response (gamma-ASSR) power has been reported in major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SZ), but distinguishing between these disorders based solely on power remains challenging. Directed functional connectivity (DFC), which captures topological patterns of causal information flow, may provide more diagnostic-specific markers. However, conventional case-control framework often disregards the substantial individual heterogeneity, yielding unreliable biomarkers.
View Article and Find Full Text PDFJ Neurochem
September 2025
Department of Biology and Biotechnologies "Charles Darwin", Sapienza University of Rome, Rome, Italy.
Patients with Duchenne muscular dystrophy (DMD) may experience neurobehavioral and cognitive concerns, including psychiatric symptoms, due to the absence of full-length dystrophin (Dp427), frequently accompanied by deficiencies in shorter isoforms. The lack of dystrophin affects neurophysiological processes from the uterine phase, impacting neural circuitry in brain regions such as the prefrontal cortex, hippocampus, and cerebellum. This leads to reduced inhibitory GABAergic transmission and altered hippocampal glutamatergic signaling.
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