ArticlePsychoradiology2025
Abnormal arteriolar blood volume measured by 3D inflow-based vascular-space-occupancy (iVASO) MRI and resting-state BOLD fluctuations at 7 T in individuals with recent-onset schizophrenia.
Article in Psychoradiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: We previously reported lower baseline arteriolar cerebral blood volumes (CBVa) in almost all gray matter regions in a cohort of individuals with schizophrenia of varying ages and disease duration. The extent to which decreased CBVa is also present in recent-onset schizophrenia, and how this impacts neurovascular coupling, remains to be determined. In this study, we sought to determine the extent of CBVa deficits in recent-onset schizophrenia and the relationship of CBVa to region-specific resting-state neural activity. Methods: Using 7 T MRI, CBVa was measured in 90 regions using 3D inflow-based vascular-space-occupancy (iVASO) imaging in 16 individuals with recent-onset schizophrenia (disease duration: x̄ = 1.18 ± 1.4 years) and 12 age-matched controls. Resting-state functional MRI (rs-fMRI) was used to determine fractional amplitudes of low-frequency fluctuations (fALFF) and intrinsic connectivity (ICC) in spontaneous blood oxygen level-dependent (BOLD) signal. The region-specific relationship between CBVa and fALFF was determined as an index of neurovascular coupling. Results: Compared with healthy participants, CBVa was lower in individuals with schizophrenia in almost all brain regions, with a global effect size of 0.23 and regional effect sizes up to 0.41. Individuals with schizophrenia also exhibited lower fALFF diffusely across cortical and subcortical gray matter regions. Ratios of mean regional CBVa to fALFF and ICC were significantly lower in patients in numerous brain regions. Conclusion: These findings indicate that early-stage schizophrenia is characterized by widespread microvascular abnormalities and associated resting-state deficits in neural activity, suggesting that abnormalities in neurovascular coupling may contribute to the pathophysiology of schizophrenia.
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