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Background and Purpose: Recent studies revealed that inflammation contributes to plaque instability. Cyclo-oxygenase (COX)-2 is one of the key enzymes in plaque inflammation. We examined the relation between a polymorphism in the COX-2 gene and carotid plaque echogenicity in patients with high risk of cerebrovascular disease to evaluate the involvement of COX-2 in plaque instability. Methods: The study comprised 469 individuals with carotid atherosclerotic plaques. We quantified the echogenicity of the largest plaque in each participant by integrated backscatter analysis. The –765G > C variant of the COX-2 gene was genotyped by restriction enzyme fragment length polymorphism analysis. Urinary 6-keto prostaglandin F1α levels and flow-mediated dilation were measured in 25 participants from the –765GC genotype group and 25 matched participants from the –765GG genotype group. Results: The carotid plaque echogenicity in the variant genotype group (n = 44) was lower than that in the –765GG genotype group (n = 425, p = 0.017). The association remained significant when we controlled for atherosclerotic risk factors, plaque thickness and serum levels of interleukin-6 (p = 0.027). The level of urinary 6-keto prostaglandin F1α and flow-mediated dilation in the variant genotype group was significantly lower than that in the –765GG genotype group. Conclusions: The –765G > C variant of COX-2 was associated with reduced carotid plaque echogenicity in Japanese. Diminished COX-2 activity in the endothelium may contribute to plaque instability. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Subcortical ischemic vascular dementia (SVD) caused by small-artery disease is a major cause of dementia. It still remains unclear, however, whether SVD may present with localized regional cerebral blood flow (rCBF) changes. We aimed to clarify the local rCBF changes associated with dementia in patients with early-stage SVD. Methods: The subjects consisted of 15 patients with early-stage SVD [Mini Mental State Examination (MMSE) score: 20 ± 3.5] without apparent brain atrophy (SVD group), 11 patients without dementia with white matter lesions (non-dementia-WML group) and 16 age-matched controls. All the subjects were right-handed and underwent brain perfusion single photon emission computed tomography (SPECT), magnetic resonance imaging and cognitive function testing. Statistical analysis of the differences in the SPECT rCBF was performed by SPM2. The degree of severity of the WMLs was evaluated based on the Scheltens rating scale. Results: The results of SPM analysis revealed that the rCBF in the SVD group was significantly decreased in the pulvinar nuclei of the thalamus of both sides as compared with that in the controls, and in the left pulvinar nucleus as compared with that in the non-dementia-WML group. On the other hand, SPM analysis revealed no significant reduction in rCBF in the non-dementia-WML group as compared with that in the controls. The WMLs in the left parietal region were severer in the SVD group than in the non-dementia-WML group. Conclusions: In patients with early-stage SVD without apparent brain atrophy, significant rCBF reduction in the bilateral pulvinar nuclei as compared with that in normal controls, and in the left pulvinar nucleus as compared with that in patients without dementia with WMLs was found. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Introduction: The primary objective of this study was to elucidate the predictive role of subtle motor impairment evaluated using the Unified Parkinson’s Disease Rating Scale (UPDRS) Part III on mortality and functional outcome. The secondary objective was to evaluate the association of motor impairment with small vessel disease (SVD) severity. Methods: We derived data from a Japanese cohort of patients with evidence of SVD who were enrolled from 2015 to 2019, and followed until 2023. The present study included 586 participants who agreed for UPDRS Part III evaluation. The severity of white matter hyperintensities (WMHs) and the presence of lacunes were evaluated. Cox proportional hazard models and multiple logistic regression analysis were used to examine the association between UPDRS Part III score and all-cause death and functional outcome defined by the modified Rankin Scale (mRS) score at the last visit, respectively. Results: The median age was 71 years, and the median UPDRS Part III score was 2. The UPDRS Part III score was associated with the severity of WMH (r = 0.225, p < 0.001) and the number (0, 1, ≥2) of lacunes (p < 0.001). During a mean follow-up period of 4.8 years, 29 patients died. The Cox proportional hazard analysis revealed that high UPDRS Part III scores (≥5) were associated with a higher risk of all-cause death compared to low (score 0) and middle (score 1–4) scores (adjusted hazard ratio 3.04; 95% confidence interval, 1.50–7.34, p = 0.005). In multivariate logistic analysis, high UPDRS Part III scores were associated with poor functional outcome (mRS of ≥3) compared with low and middle scores after adjusting for confounding factors (adjusted odds ratio 1.86; 95% confidence interval 1.02–3.41, p = 0.043). Conclusions: Subtle motor impairment was associated with the severity of WMH and number of lacunes and could predict mortality and poor functional outcome independently of vascular risk factors and severity of WMH and lacunes. [ABSTRACT FROM AUTHOR]