Deficit schizophrenia (DS), characterized by persistent and primary negative symptoms, is considered a promising homogeneous subtype of schizophrenia. According to the disconnection hypothesis, abnormalities in white matter fibers are common in schizophrenia. However, comprehensive measurement of white matter metrics and exploration of the relationships between neuroanatomical changes and cognitive functions in DS patients are still unknown. A cross-sectional study was conducted, including 35 DS patients, 37 non-deficit schizophrenia (NDS) patients, and 39 healthy controls (HC), all male and matched for age and education level. The tract-based spatial statistics method was performed to detect differences in fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD) and radial diffusivity (RD) among these three groups. Cognitive function in DS and NDS patients was assessed using the Mini-Mental State Examination (MMSE) and Mattis Dementia Rating Scale. Correlation analyses were performed between diffusion metrics in regions showing differences and clinical scales. The results showed significant differences in diffusion metrics (FA, RD, AD, MD) across DS, NDS, and HC groups, particularly in the corpus callosum, corona radiata, and thalamic radiations. Compare to NDS, DS patients exhibited more reductions in FA and increases in RD, especially in the right posterior thalamic radiation and right superior longitudinal fasciculus. Correlation analysis revealed that lower FA in specific regions was linked to worse cognitive and clinical symptoms. These findings reinforce the dysconnectivity hypothesis of schizophrenia and highlight the distinct pathological mechanisms of white matter impairments in DS. Correlations in crucial white matter regions suggest disruptions in thalamo-cortical feedback loops, potentially contributing to the cognitive impairments observed. This provides a deeper understanding of how structural brain changes relate to clinical symptoms.
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http://dx.doi.org/10.1016/j.jpsychires.2024.11.054 | DOI Listing |
Cell Rep
January 2025
Michael Smith Laboratories, University of British Columbia, Vancouver, BC V6T 1Z4, Canada; Department of Medical Genetics, University of British Columbia, Vancouver, BC V6T 1Z3, Canada; Program in Neurosciences and Mental Health, Hospital for Sick Children, Toronto, ON M5G 0A4, Canada; Institute of Medical Science, University of Toronto, Toronto, ON M5S 1A8, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ON M5S 1A8, Canada. Electronic address:
Here, we used single cell RNA sequencing and single cell spatial transcriptomics to characterize the forebrain neural stem cell (NSC) niche under homeostatic and injury conditions. We defined the dorsal and lateral ventricular-subventricular zones (V-SVZs) as two distinct neighborhoods and showed that, after white matter injury, NSCs are activated to make oligodendrocytes dorsally for remyelination. This activation is coincident with an increase in transcriptionally distinct microglia in the dorsal V-SVZ niche.
View Article and Find Full Text PDFNeuroimage Rep
December 2024
Department of Pediatrics, Division of Developmental-Behavioral Pediatrics, Stanford University, Stanford, CA, USA.
Background: Severe neonatal inflammatory conditions in very preterm infants (VPT: <32 weeks gestational age, GA) are linked to adverse neurodevelopmental outcomes. Differences in white matter (WM) microstructure of the corpus callosum (CC) have been observed at age 6 in VPT children with a history of severe neonatal inflammation. The goal of this study was to determine whether these CC differences can be detected at term-equivalent age using diffusion MRI (dMRI), and whether neonatal inflammation is associated with altered WM in additional tracts implicated in the encephalopathy of prematurity.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Laboratory of Epidemiology and Population Sciences, National Institute on Aging, NIA/NIH/IRP, Baltimore, Maryland, USA.
Introduction: The plasma proteome's mediating or moderating roles in the association between poor cardiovascular health (CVH) and brain white matter (WM) microstructural integrity are largely unknown.
Methods: Data from 3953 UK Biobank participants were used (40-70 years, 2006-2010), with a neuroimaging visit between 2014 and 2021. Poor CVH was determined using Life's Essential 8 (LE8) and reversing standardized z-scores (LE8 ).
Ann Neurol
January 2025
Centre for Clinical Brain Sciences, Edinburgh Imaging, UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK.
Objective: After a recent small subcortical infarct (RSSI), some patients develop perilesional or remote hyperintensities ('caps/tracks') to the index infarct on T2/FLAIR MRI. However, their clinical relevance remains unclear. We investigated the clinicoradiological correlates of 'caps/tracks', and their impact on long-term outcomes following RSSI.
View Article and Find Full Text PDFCerebellum
January 2025
Department of Neurology, Donders Institute for Brain, Cognition & Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
Repeat expansions in the fibroblast growth factor 14 gene (FGF14), associated with spinocerebellar ataxia type 27B (SCA27B), have emerged as a prevalent cause of previously unexplained late-onset cerebellar ataxia. Here, we present a patient with residual symptom of gait ataxia after complicated meningioma surgery, who presented with progressive symptoms of oculomotor disturbances, speech difficulties, vertigo and worsening of gait imbalance, twelve years post-resection. Neuroimaging revealed a surgical resection cavity in the dorsolateral side of the left cerebellar hemisphere, accompanied by gliosis in left cerebellar hemisphere extending into the vermis, extensive non-specific supratentorial periventricular white matter abnormalities, and mild atrophy of the cerebellar vermis.
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