Measurement of carotid plaque volume and its progression are important tools for research and patient management. In this study, we investigate the observer variability in the measurement of plaque volume as determined by 3-dimensional (3D) ultrasound (US). We also investigate the effect of interslice distances (ISD) and repeated 3D US scans on measurement variability. Materials and Methods Forty 3D US patient images of plaques (range, 37.43 to 604.1 mm3) were measured by manual planimetry. We applied ANOVA to determine plaque volume measurement variability and reliability. Plaque volumes were measured with 9 ISDs to determine the effect of ISD on measurement variability. Additional plaque volumes were also measured from multiple 3D US scans to investigate repeated scan acquisition variability. Results Intraobserver and interobserver measurement reliabilities were 94% and 93.2%, respectively. Plaque volume measurement variability decreased with increasing plaque volume (range, 27.1% to 2.2%). Measurement precision was constant for ISDs between 1.0 and 3.0 mm, whereas plaque volume measurement variability increased with ISD. Repeated 3D US scan measurements were not different from single-scan measurements (P=0.867). Conclusions The coefficient of variation in the measurement of plaque volume decreased with plaque size. The volumetric change that must be observed to establish with 95% confidence that a plaque has undergone change is approximately 20% to 35% for plaques <100 mm3 and approximately 10% to 20% for plaques >100 mm3. Measurement precision was unchanged for ISDs <3.0 mm, whereas measurement variability increased with ISD. Repeated 3D US scans did not affect plaque volume measurement variability.
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http://dx.doi.org/10.1161/01.STR.0000121161.61324.ab | DOI Listing |
Alzheimers Dement
December 2024
Gladstone Institutes, UCSF, San Francisco, CA, USA.
Background: Cerebrovascular alterations and innate immune activation are key features of Alzheimer's disease (AD). However, the mechanisms that link blood-brain barrier disruption to neurodegeneration are poorly understood and well-defined druggable targets at the neurovascular interface are limited.
Method: By developing a multiomic and genetic loss-of-function pipeline, we reported the transcriptomic and global phosphoproteomic landscape of blood-induced microglia activation and the causal role for fibrin in induction of neurodegenerative genes and oxidative stress pathways in innate immune cells.
Alzheimers Dement
December 2024
McGill University, Montreal, QC, Canada.
Background: Despite amyloid-β (Aβ) plaques and tau neurofibrillary tangles being recognized as major Alzheimer's Disease (AD) hallmarks, their synergistic contribution to neuronal activity remains unclear. We developed a neuroimaging-based personalized brain activity model to assess the in-vivo functional impact of AD pathophysiology. In previous reports, model-inferred neuronal excitability predicted disease progression (i.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Western Ontario, London, ON, Canada.
Background: Apolipoprotein E (ApoE) exhibits isoform-specific interactions with Alzheimer's disease (AD)-related pathology. In comparison with the more common ApoE3 isoform, ApoE4 promotes amyloid-β (Aβ) deposition, enhances tau-mediated neurodegeneration and inflammation. However, the lack of appropriate preclinical models has limited the ability to evaluate the potential synergistic effect of Aβ, tau and ApoE on cognition and disease progression.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of California, Irvine, Irvine, CA, USA.
Background: Condensed extracellular matrix structures called perineuronal nets (PNNs) preferentially enwrap the soma and stabilize proximal synapses of parvalbumin-expressing inhibitory neurons in the cortex, serving as a protective barrier against neurotoxins. While PNN structural integrity declines in the healthy aging brain, this reduction is exacerbated in Alzheimer's disease (AD). In the 5xFAD mouse model of amyloidosis, the elimination of microglia prevents reductions in PNN, suggesting microglia are responsible for the over-degradation of PNNs observed in AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Illinois Institute of Technology, Chicago, IL, USA.
Background: Elevated iron in brain is a source of free radicals that causes oxidative stress which has been linked to neuropathologies and cognitive impairment among older adults. The aim of this study was to investigate the association of iron levels with transverse relaxation rate, R, and white matter hyperintensities (WMH), independent of the effects of other metals and age-related neuropathologies.
Method: Cerebral hemispheres from 437 older adults participating in the Rush Memory and Aging Project study (Table 1) were imaged ex-vivo using 3T MRI scanners.
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