Background: Deficits in the differentiation of negative emotions - the ability to specifically identify one's negative emotions - are associated with poorer mental health outcomes. However, the processes that lead to individual differences in negative emotion differentiation are not well understood, hampering our understanding of why this process is related to poor mental health outcomes. Given that disruptions in some affective processes are associated with white matter microstructure, identifying the circuitry associated with different affective processes can inform our understanding of how disturbances in these networks may lead to psychopathology. Thus, examination of how white matter microstructure relates to individual differences in negative emotion differentiation (NED) may provide insights into (i) its component processes and (ii) its relationship to brain structure.
Method: The relationship between white matter microstructure and NED was examined.
Results: NED was related to white matter microstructure in right anterior thalamic radiation and inferior fronto-occipital fasciculus and left peri-genual cingulum.
Limitations: Although participants self-reported psychiatric diagnoses and previous psychological treatment, psychopathology was not directly targeted, and thus, the extent to which microstructure related to NED could be examined in relation to maladaptive outcomes is limited.
Conclusions: Results indicate that NED is related to white matter microstructure and suggest that pathways subserving processes that facilitate memory, semantics, and affective experience are important for NED. Our findings provide insights into the mechanisms by which individual differences in NED arise, suggesting intervention targets that may disrupt the relationship between poor differentiation and psychopathology.
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http://dx.doi.org/10.1016/j.jad.2023.04.010 | 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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