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Background: White matter hyperintensities (WMH) are a key imaging feature of cerebral small-vessel disease (CSVD). However, there is a lack of standardized methods for determining WMH volume, and the value of total white matter (WM) volume in the assessment of cognitive impairment in patients with CSVD remains unknown. Objective:We aimed to explore the correlations of WMH volume andWM volume with cognitive dysfunction and its components in patients with CSVD. We also aimed to compare the value of the Fazekas score, WMH volume, and ratio of WMH volume to total WM volume in the assessment of cognitive dysfunction. Methods: The study included 99 patients with CSVD. Patients were categorized into following groups based on MoCA scores: patients with mild cognitive impairment and those without. Brain magnetic resonance images were processed to investigate differences in WMH and WM volumes between the groups. Logistic regression analysis was used to determine whether these two factors were independent risk factors for cognitive dysfunction. Correlation analysis was used to examine the relationships of WMH and WM volume with different types of cognitive impairment. Receiver operating characteristic curves were used to compare the effectiveness of the WMH score, WMH volume, and WMH to WM ratio for evaluating cognitive dysfunction. Results: There were significant differences in age, education level, WMH volume, and WM volume between the groups (P < 0.05). After adjusting for age and education, the multivariate logistic analysis indicated that both WMH volume and WM volume were independent risk factors for cognitive dysfunction. Correlation analysis indicated that WMH volume was mainly related to cognition involving the visual space and delayed recall. WM volume was not strongly associated with different types of cognitive dysfunction. The WMH to WM ratio was the strongest predictor, with an area under the curve value of 0.800 and a 95% confidence interval of 0.710-0.891. Conclusion: Increases in WMH volume may aggravate cognitive dysfunction in patients with CSVD, and a higher WM volume may reduce the effect of WMH volume on cognitive function to a certain extent. The ratio of WMH to total WM volume may reduce the impact of brain atrophy, allowing for more accurate evaluation of cognitive dysfunction in older adults with CSVD. [ABSTRACT FROM AUTHOR]

• CSVD is highly prevalent in geriatric outpatients. • CSVD is associated with increased mortality risk. • This association is independent of important confounders. • This association is robust amongst subgroups. Cerebral Small-Vessel Disease (CSVD) is a complex condition affecting the brain's vascular network, linked to cognitive and physical decline, cerebrovascular disease, and death. This study assesses the relationship between CSVD (composite and individual features) and all-cause mortality in a large cohort of geriatric outpatients. Data from 1305 geriatric outpatients (mean age 78 ± 7; 51 % female) in the Amsterdam Ageing cohort were analysed. CSVD presence was based on brain imaging (MRI or CT), defined by a Fazekas score ≥ 2, presence of ≥1 lacunes, or (in MRI) ≥ 3 microbleeds. Mortality data (February 2016 - January 2024) was sourced from the Dutch Municipality Register. The relationship between CSVD and all-cause mortality was evaluated using a Cox proportional-hazards model, adjusting for key confounders. At baseline, 835 (64 %) of the 1305 patients had CSVD. During a median follow-up of 3.1 years (IQR 1.6–4.6 years), all-cause mortality was 40 % (333 patients) in the CSVD group and 26 % (121 patients) in the non-CSVD group, corresponding with incidence rates of 137 and 78 per 1000 patient-years, respectively. The age- and sex-adjusted hazard ratio for mortality in the CSVD group was 1.6 (95 % CI: 1.3–2.0). This association remained significant after adjusting for cardiovascular disease and its risk factors, physical function (gait speed), and cognitive function (MMSE). Radiographic CSVD presence is prevalent and its integration into daily care is important as it is independently linked to increased all-cause mortality in geriatric outpatients. [Display omitted] [ABSTRACT FROM AUTHOR]

Background: White-matter hyperintensity (WMH) is the key magnetic resonance imaging (MRI) marker of cerebral small-vessel disease (CSVD). This study aimed to investigate whether habitat analysis based on physiologic MRI parameters can predict the progression of WMH and cognitive decline in CSVD., Methods: Diffusion- and perfusion-weighted imaging data were obtained from 69 patients with CSVD at baseline and at 1-year of follow-up. The white-matter region was classified into constant WMH, growing WMH, shrinking WMH, and normal-appearing white matter (NAWM) according to the T2-fluid-attenuated inversion recovery (FLAIR) sequences images at the baseline and follow-up. We employed k-means clustering on a voxel-wise basis to delineate WMH habitats, integrating multiple diffusion metrics and cerebral blood flow (CBF) values derived from perfusion data. The WMH at the baseline and the predicted WMH from the habitat analysis were used as regions of avoidance (ROAs). The decreased rate of global efficiency for the whole brain structural connectivity was calculated after removal of the ROA. The association between the decreased rate of global efficiency and Montreal Cognitive Assessment (MoCA) and mini-mental state examination (MMSE) scores was evaluated using Pearson correlation coefficients., Results: We found that the physiologic MRI habitats with lower fractional anisotropy and CBF values and higher mean diffusivity, axial diffusivity, and radial diffusivity values overlapped considerably with the new WMH (growing WMH of baseline) after a 1-year follow-up; the accuracy of distinguishing growing WMH from NAWM was 88.9%±12.7% at baseline. Similar results were also found for the prediction of shrinking WMH. Moreover, after the removal of the predicted WMH, a decreased rate of global efficiency had a significantly negative correlation with the MoCA and MMSE scores at follow-up., Conclusions: This study revealed that a habitat analysis combining perfusion with diffusion parameters could predict the progression of WMH and related cognitive decline in patients with CSVD., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-24-238/coif). The authors have no conflicts of interest to declare., (2024 Quantitative Imaging in Medicine and Surgery. All rights reserved.)

Background: According to population-based studies, microalbuminuria is associated with subsequent cognitive decline over a 4–6-year period, because of cerebral small-vessel disease (CSVD). This prospective cross-sectional study (NCT02852772) was designed to evaluate whether a history of microalbuminuria is associated with subsequent cognitive decline in combined antiretroviral therapy (cART)-treated persons living with human immunodeficiency virus (PLHIVs). Methods: From our computerized medical database, we identified 30 PLHIVs (median age 52 years), immunovirologically controlled on cART, who had microalbuminuria in 2008 and had undergone, between 2013 and 2015, a comprehensive neuropsychological assessment (NPA) including seven domains (cases): information-processing speed, motor skills, executive functions, attention/working memory, learning/memory, reasoning and verbal fluency. Forty-nine PLHIVs matched for age (median age 48 years; p = 0.19), sex, and year of first HIV-seropositivity without microalbuminuria in 2008 were identified and underwent the same NPA between 2013 and 2015 (controls). Results: Cases performed less well than controls for information-processing speed (p = 0.01) and motor skills (p = 0.02), but no differences were found for the other cognitive domains and global z-scores. A multivariable linear-regression model adjusted for confounding factors confirmed the microalbuminuria effect for the information-processing-speed z score. Conclusion: cART-treated PLHIVs with a history of microalbuminuria subsequently had worse cognitive performances for the information-processing-speed domain, possibly because of CSVD. Our observations should be considered preliminary findings of a temporal link between microalbuminuria, CSVD, and subsequent cognitive impairment. [ABSTRACT FROM AUTHOR]

Lacunar infarction, white matter hyperintensities (WMH), deep cerebral microbleeds (dCMB), and deep intracerebral hemorrhage (ICH) are increasingly recognized as manifestations of a common underlying vasculopathy, encompassed by the term "cerebral small-vessel disease" (CSVD). Epidemiologic studies have found robust associations of the individual aspects of CSVD with aging and hypertension; however, heritability estimates and the disproportionate burden of CSVD in underrepresented minorities suggest that genetic factors contribute substantially to CSVD risk. Here we present the rationale for studying these phenotypes as part of a spectrum of CSVD, review aspects of genetic study design, summarize current knowledge of genetic contribution to CSVD, and discuss the next steps required to translate these genetic discoveries into therapies for this devastating disease. Genetic studies were identified using PubMed. Regions achieving genome-wide significance in association studies, meta-analyses of candidate gene studies, and studies of genes associated with Mendelian conditions exhibiting CSVD phenotypes have been summarized.

Background: Cerebral microbleeds (CMBs) are small cerebrovascular lesions. More and more CMBs have been found in patients with ischemic stroke, dementia, and cerebral amyloid angiopathy, as well as some normal elderly populations. The objective of this study is to summarize the main risk factor, impairment, and therapy of CMBs.Methods: We searched and scanned all the literature with the keyword "cerebral microbleeds" or "CMBs" in the database of PubMed and Elsevier.Results: The risks factors for CMBs are complicated, including those that cause large-vessel disease, such as hypertension and old age, and those that cause small-vessel disease, such as amyloid deposits, endothelial lesions, and atrial fibrillation. Moreover, drugs and therapies used to treat cerebrovascular diseases such as statin, intravenous thrombolysis, and coumarin may also increase risk of CMBs. The relationship between antiplatelet treatment and CMBs is now unclear. Gene polymorphisms have been considered to be associated with CMBs. Gene mutations involving collagen type IV alpha 1 and collagen type IV alpha 2, sortilin-related receptor gene, forkhead box C1, and paired-like homeodomain 2 were reported to affect CMBs with the modification of corresponding proteins and functions. The cognition impairment caused by CMBs draws great attention. White matter deterioration is the possible answer. However, different studies could not reach the same conclusion on the damage of cognition of CMBs.Conclusions: Further research is needed to provide effectual therapeutic proposals for CMBs, which differ from the treatment for large-artery disease and dementia. [ABSTRACT FROM AUTHOR]

Background: Decreased hemoglobin levels increase the risk of developing dementia among the elderly. However, the underlying mechanisms that link decreased hemoglobin levels to incident dementia still remain unclear, possibly due to the fact that few studies have reported on the relationship between low hemoglobin levels and neuroimaging markers. We, therefore, investigated the relationships between decreased hemoglobin levels, cerebral small-vessel disease (CSVD), and cortical atrophy in cognitively healthy women and men.Methods: Cognitively normal women (n = 1,022) and men (n = 1,018) who underwent medical check-ups and magnetic resonance imaging (MRI) were enrolled at a health promotion center. We measured hemoglobin levels, white matter hyperintensities (WMH) scales, lacunes, and microbleeds. Cortical thickness was automatically measured using surface based methods. Multivariate regression analyses were performed after controlling for possible confounders.Results: Decreased hemoglobin levels were not associated with the presence of WMH, lacunes, or microbleeds in women and men. Among women, decreased hemoglobin levels were associated with decreased cortical thickness in the frontal (Estimates, 95% confidence interval, -0.007, (-0.013, -0.001)), temporal (-0.010, (-0.018, -0.002)), parietal (-0.009, (-0.015, -0.003)), and occipital regions (-0.011, (-0.019, -0.003)). Among men, however, no associations were observed between hemoglobin levels and cortical thickness.Conclusion: Our findings suggested that decreased hemoglobin levels affected cortical atrophy, but not increased CSVD, among women, although the association is modest. Given the paucity of modifiable risk factors for age-related cognitive decline, our results have important public health implications. [ABSTRACT FROM AUTHOR]

Background: The present study aimed to evaluate the frequency of silent cerebral small-vessel disease, especially lacunes and white matter hyperintensities, in patients with or without the impaired glucose tolerance (IGT) and type-2 diabetes mellitus, and to characterize the diabetes-correlated factors related to silent cerebral small-vessel disease., Methods: This is a retrospective cross-sectional study. Totally 698 patients were included in this study, from January 2014 to December 2019, among which 270 patients were included in the diabetes mellitus group, 106 patients were included in the IGT group, and 322 patients were included in the Control group. All patients underwent magnetic resonance imaging to investigate the silent cerebral small-vessel disease: the lacunes and the white matter hyperintensities. All the baseline information and diabetes-related factors, such as glycated hemoglobin level, insulin usage, etc., were collected. Then correlation analysis and regression analysis were used to explore the correlation between diabetes with related risk factors and silent cerebral small-vessel disease., Results: Lacunes and white matter hyperintensities were more common in the diabetes mellitus group than in the IGT group and the Control group, with an occurrence of lacunes of 83.3% vs. 70.8% vs. 70.4% (P=0.003), respectively, and an occurrence of white matter hyperintensities of 41.1% vs. 24.5% vs. 31.1% (P=0.003), respectively. The occurrence of lacunes was correlated with the duration of diabetes mellitus [odds ratio (OR) =1.483, 95% confidence interval (CI): 1.082-2.031, P=0.009] and the age (OR =1.141, 95% CI: 1.102-1.180, P<0.001), while white matter hyperintensities were independently correlated only with the age (OR =1.124, 95% CI: 1.094-1.155, P<0.001)., Conclusions: Lacunes and white matter hyperintensities, are more common in the diabetes mellitus patients than in the IGT patients or in the other patients. The occurrence of lacunes was correlated with the duration of diabetes mellitus and the age, while the occurrence of white matter hyperintensities was independently correlated with the age., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-21-786/coif). The authors have no conflicts of interest to declare., (2022 Quantitative Imaging in Medicine and Surgery. All rights reserved.)

Background: Decreased hemoglobin levels increase the risk of developing dementia among the elderly. However, the underlying mechanisms that link decreased hemoglobin levels to incident dementia still remain unclear, possibly due to the fact that few studies have reported on the relationship between low hemoglobin levels and neuroimaging markers. We, therefore, investigated the relationships between decreased hemoglobin levels, cerebral small-vessel disease (CSVD), and cortical atrophy in cognitively healthy women and men., Methods: Cognitively normal women (n = 1,022) and men (n = 1,018) who underwent medical check-ups and magnetic resonance imaging (MRI) were enrolled at a health promotion center. We measured hemoglobin levels, white matter hyperintensities (WMH) scales, lacunes, and microbleeds. Cortical thickness was automatically measured using surface based methods. Multivariate regression analyses were performed after controlling for possible confounders., Results: Decreased hemoglobin levels were not associated with the presence of WMH, lacunes, or microbleeds in women and men. Among women, decreased hemoglobin levels were associated with decreased cortical thickness in the frontal (Estimates, 95% confidence interval, -0.007, (-0.013, -0.001)), temporal (-0.010, (-0.018, -0.002)), parietal (-0.009, (-0.015, -0.003)), and occipital regions (-0.011, (-0.019, -0.003)). Among men, however, no associations were observed between hemoglobin levels and cortical thickness., Conclusion: Our findings suggested that decreased hemoglobin levels affected cortical atrophy, but not increased CSVD, among women, although the association is modest. Given the paucity of modifiable risk factors for age-related cognitive decline, our results have important public health implications.