Objective: Hyperacute stroke affects various patient subgroups who may benefit from different management strategies. Magnetic resonance imaging (MRI) quantitative susceptibility mapping (QSM) is a recent MRI technique for measuring deoxyhemoglobin levels. The results of QSM thus have the potential to act as a quantitative biomarker for predicting the success of endovascular interventions.
Methods: Twenty-five patients with M1 occlusions were evaluated retrospectively. QSM measurements were obtained based on susceptibility-weighted imaging sequences from the most prominent veins in each of the four standard regions of interest: the cortical and thalamostriate veins ipsilateral and contralateral to the side of the stroke. The results were analyzed using Wilcoxon’s signed rank test and compared with presenting National Institutes of Health stroke scale (NIHSS) score.
Results: Cortical veins ipsilateral to the stroke showed the greatest elevation in susceptibility compared with all other vein groups. Both ipsilateral and contralateral thalamostriate vein susceptibilities showed strong inverse correlation with presenting NIHSS score.
Conclusion: Thalamostriate vein susceptibility shows a strong inverse correlation with presenting NIHSS in adult patients with hyperacute stroke who are selected for endovascular intervention by advanced imaging.
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http://dx.doi.org/10.1177/0300060519832462 | DOI Listing |
J Neurosci Methods
January 2025
Neuroimage Analytics Laboratory and Biggs Institute Neuroimaging Core, Glenn Biggs Institute for Neurodegenerative Disorders, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA; Research Imaging Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA. Electronic address:
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Washington University School of Medicine, Saint Louis, MO, USA.
Background: The recent European-ancestry based genome-wide association study (GWAS) of Alzheimer disease (AD) by Bellenguez2022 has identified 75 significant genetic loci, but only a few have been functionally mapped to effector gene level. Besides the large-scale RNA expression, protein and metabolite levels are key molecular traits bridging the genetic variants to AD risk, and thus we decided to integrate them into the genetic analysis to pinpoint key proteins and metabolites underlying AD etiology. Few studies have generated more than one layer of post-transcriptional phenotypes, limiting the scale of biological translation of disease modifying treatments.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Stevens Neuroimaging and Informatics Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Background: Microglia undergo varying regional dependent functional changes, which can exacerbate cognitive decline in Alzheimer's disease, but the full clinical relevance remains unclear. Ramified microglia survey the micro-environment and inert/amoeboid microglia engulf debris. A third morphological type; rod microglia, have been observed in a number of pathological conditions, but are relatively understudied.
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December 2024
Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, TN, USA.
Background: The Apolipoprotein E ε4 (APOE-ε4) allele is common in the population, but acts as the strongest genetic risk factor for late-onset Alzheimer's disease (AD). Despite the strength of the association, there is notable heterogeneity in the population including a strong modifying effect of genetic ancestry, with the APOE-ε4 allele showing a stronger association among individuals of European ancestry (EUR) compared to individuals of African ancestry (AFR). Given this heterogeneity, we sought to identify genetic modifiers of APOE-ε4 related to cognitive decline leveraging APOE-ε4 stratified and interaction genome-wide association analyses (GWAS).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The University of Texas at San Antonio, San Antonio, TX, USA.
Background: Neurodegeneration is characterized by the progressive loss of neurons. However, the mechanisms by which neurons die in Alzheimer's disease (AD) remain elusive. Disrupted iron homeostasis is associated with accelerated cognitive decline, amyloid beta deposition, and AD progression, but its pathogenic relevance is poorly understood.
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