CSVDClustering and Singular Value Decomposition (computing)
CSVDChrysanthemum Stunt Viroid
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Logistic regression was used to evaluate the relationship between Cav-1 and cSVD by calculating adjusted odds ratios (OR) and 95% confidence intervals (CI).
For ischemic cSVD, patients with SLIs were older than patients without (65.0 [+ or -] 8.7 versus 61.2 [+ or -] 9.2, P = 0.009).
Relationship between Cav-1 and cSVD. After adjusting for age and sex (model 1), presence of CMBs in patients with low Cav-1 level ([less than or equal to] 5.25 ng/mL) was higher (OR = 3.69,95% CI 1.78-7.64, P = 0.00044) than that in patients with high Cav-1 level (>5.25 ng/mL).
These molecular mechanisms are also supposed to be associated with the occurrence of cSVD. As found in this clinical study, lower serum Cav-1 levels were associated with the presence of CMBs.
CMBs, as a novel image surrogate of cSVD, have been proved to be associated with endothelial dysfunction, BBB leakage, inflammation activation, and oxidative stress [7, 13, 19, 26].
For ischemic cSVD, there were no remarkable associations between serum Cav-1 levels and SLIs or WMHs in this study.
These results support the notion that EPVS in the BG may be a marker of CSVD.[22],[28] The results of a prospective cohort study showed that WM-EPVS was associated with cerebral amyloid angiopathy (CAA) and superficial siderosis.[29] Conversely, a prospective, multicenter, hospital-based study published by Zhang et al .[30] showed that hypertension was an independent risk factor for EPVS in WM but not in BG or hippocampus.
Patients with a high degree of EPVS at baseline experience greater declines in processing speed and have an increased likelihood of developing vascular dementia.[31] Huijts et al .[32] conducted a 5-year study of 189 patients with a high risk of CSVD and found that an increase in BG-EPVS was associated with a decrease in information processing speed and that this relationship was independent of age and WML.
LI is usually considered benign and appropriate secondary preventive measures are, therefore, often neglected despite the fact that LI is associated with a higher risk of subsequent stroke and dementia.[37] Indeed, the impact of CSVD on dementia could be much more substantial than the impact of cerebral large vessel disease.
Studies in the literature have confirmed that multiple hypertensive vasculopathies and changes in inflammatory status play pivotal roles in the pathological mechanisms underlying CSVD. The neuroimaging markers for CSVD, including WML, EPVS, LI, and CMB, have independent or combined effects on cognitive impairment.