Effects Of Cerebral Small Vessel Disease Research Articles

White Matter Free Water Outperforms Cerebral Small Vessel Disease Total Score in Predicting Cognitive Decline in Persons with Mild Cognitive Impairment.

Vascular pathology is an important partner of Alzheimer's disease (AD). Both total cerebral small vessel disease (CSVD) score and white matter free water (FW) are useful markers that could reflect cerebral vascular injury. We aim to investigate the efficacy of these two metrics in predicting cognitive declines in patients with mild cognitive impairment (MCI). We enrolled 126 MCI subjects with 3D T1-weighted images, fluid-attenuated inversion recovery images, T2* images, diffusion tensor imaging images, cerebrospinal fluid biomarkers and neuropsychological tests from the Alzheimer's Disease Neuroimaging Initiative database. The total CSVD score and FW values were calculated. Simple and multiple linear regression analyses were applied to explore the association between vascular and cognitive impairments. Linear mixed effect models were constructed to investigate the efficacy of total CSVD score and FW on predicting cognitive decline. FW was associated with baseline cognition and could predict the decline of executive and language functions in MCI subjects, while no association was found between total CSVD score and cognitive declines. FW is a promising imaging marker for investigating the effect of CSVD on AD progression.

The Relationship Between ADAMTS13 Activity and Overall Cerebral Small Vessel Disease Burden: A Cross-Sectional Study Based on CSVD.

Objectives: This study aimed to investigate the association between plasma von Willebrand factor (VWF) level, ADAMTS13 activity, and neuroimaging features of cerebral small vessel disease (CSVD), including the CSVD neuroimaging markers and the overall CSVD burden.Methods: CSVD patients admitted to our hospital from 2016 to 2020 were recruited. Plasma VWF level and ADAMTS13 activity were measured. The overall effect of CSVD on the brain was described as a validated CSVD score. We evaluated the association between VWF levels, ADAMTS13 activity, and the increasing severity of CSVD score by the logistic regression model.Results: We enrolled 296 patients into this study. The mean age of the sample was 69.0 years (SD 7.0). The mean VWF level was 1.31 IU/mL, and the ADAMTS13 activity was 88.01 (SD 10.57). In multivariate regression analysis, lower ADAMTS13 activity and higher VWF level was related to white matter hyperintensity (WMH) [β = −7.31; 95% confidence interval (CI) (−9.40, −4.93); p<0.01; β = 0.17; 95% confidence interval (0.11, 0.23); p<0.01], subcortical infarction (SI) [(β = −9.22; 95% CI (−11.37, −7.06); p<0.01); β = 0.21; 95% confidence interval (0.15, 0.27); p<0.01] independently, but not cerebral microbleed (CMB) [(β = −2.3; 95% CI (−4.95, 0.05); p = 0.22); β = 0.02; 95% confidence interval (−0.05, 0.08); p = 0.63]. Furthermore, ADAMTS13 activity was independently negatively correlated with the overall CSVD burden (odd ratio = 21.33; 95% CI (17.46, 54.60); p < 0.01) after adjustment for age, history of hypertension, and current smoking.Conclusions: Reducing ADAMTS13 activity change is related to white matter hyperintensity, subcortical infarction, but not with cerebral microhemorrhage. In addition, ADAMTS13 may have played an essential role in the progression of CSVD.

Insulin Resistance Is a Risk Factor for Overall Cerebral Small Vessel Disease Burden in Old Nondiabetic Healthy Adult Population.

Background and Purpose: This study aimed to investigate the association between insulin resistance (IR) and the overall cerebral small vessel disease (CSVD) burden.Methods: We recruited elderly, nondiabetic, healthy subjects prospectively. The overall effect of CSVD on the brain was described by a validated CSVD score. The homeostasis model assessment–estimated insulin resistance index (HOMA-IR) was used for IR estimation, and HOMA-IR ≥2.80 was defined as IR. We evaluated the association between IR and the increasing severity of CSVD score by ordinal regression models adjusting for demographics and cardiovascular risk factors.Results: A total of 156 healthy participants were recruited. The mean age was older in the IR group than in the non-IR group (70.03 vs. 67.45, p = 0.04), and the prevalence of hypertension was significantly higher in the IR group than in the non-IR group (82.35% vs. 53.28%, p < 0.01). In ordinal regression analysis, IR was positively associated with increasing severity of the total CSVD score (adjusted odds ratio, 3.74; 95% confidence interval, 1.63–5.08; p < 0.01) after adjusting traditional risk factors. Furthermore, HOMA-IR levels showed a positive dose-dependent correlation with the total CSVD score (p < 0.01, p for trend <0.01).Conclusions: IR is independently associated with increasing severity of the overall CSVD burden, independent of other clinical risk factors in an elderly, nondiabetic, healthy population. Furthermore, HOMA-IR level is correlated with the CSVD burden in a dose-dependent manner.

The consequence of cerebral small vessel disease: Linking brain atrophy to motor impairment in the elderly.

In the elderly, brain structural deficits and gait disturbances due to cerebral small vessel disease (CSVD) have been well demonstrated. The relationships among CSVD, brain atrophy, and motor impairment, however, are far from conclusive. Particularly, the effect of CSVD on subcortical nuclear atrophy, motor performance of upper extremities, and associating patterns between brain atrophy and motor impairment remains largely unknown. To address these gaps, this study recruited 770 community-dwelling subjects (35-82 years of age), including both CSVD and non-CSVD individuals. For each subject, four motor tests involving upper and lower extremities were completed. High-resolution structural MRI was applied to extract gray matter (GM) volume, white matter volume, cortical thickness, surface area, and subcortical nuclear (caudate, putamen, pallidum, and thalamus) volumes. The results showed worse motor performance of lower extremities but relatively preserved performance of upper extremities in the CSVD group. Intriguingly, there was a significant association between the worse performance of upper extremities and atrophy of whole-brain GM and pallidum in the CSVD group but not in the non-CSVD group. In addition, mediation analysis confirmed a functional CSVD-to-"brain atrophy"-to-"motor impairment" pathway, that is, a mediating role of thalamic atrophy in the CSVD effect on walking speed in the elderly, indicating that CSVD impairs walking performance through damaging the integrity of the thalamus in aging populations. These findings provide important insight into the functional consequences of CSVD and highlight the importance of evaluating upper extremities functions and exploring their brain mechanisms in CSVD populations during aging.

The effects of cerebral small-vessel disease in normal-appearing white matter integrity in mild cognitive impairment: A diffusion tensor imaging study

The effects of cerebral small-vessel disease in normal-appearing white matter integrity in mild cognitive impairment: A diffusion tensor imaging study

Spatial Distribution of White-Matter Hyperintensities in Alzheimer Disease, Cerebral Amyloid Angiopathy, and Healthy Aging

White-matter hyperintensities (WMHs) detected by magnetic resonance imaging are thought to represent the effects of cerebral small-vessel disease and neurodegenerative changes. We sought to determine whether the spatial distribution of WMHs discriminates between different disease groups and healthy aging individuals and whether these distributions are related to local cerebral perfusion patterns. We examined the pattern of WMHs by T2/fluid-attenuated inversion recovery-weighted magnetic resonance imaging in 3 groups of subjects: cerebral amyloid angiopathy (n=32), Alzheimer disease or mild cognitive impairment (n=41), and healthy aging (n=29). WMH frequency maps were calculated for each group, and spatial distributions were compared by voxel-wise logistic regression. WMHs were also analyzed as a function of normal cerebral perfusion patterns by overlaying a single photon emission computed tomography atlas. Although WMH volume was greater in cerebral amyloid angiopathy and Alzheimer disease/mild cognitive impairment than in healthy aging, there was no consistent difference in the spatial distributions when controlling for total WMH volume. Hyperintensities were most frequent in the deep periventricular WM in all 3 groups. A strong inverse correlation between hyperintensity frequency and normal perfusion was demonstrated in all groups, demonstrating that WMHs were most common in regions of relatively lower normal cerebral perfusion. WMHs show a common distribution pattern and predilection for cerebral WM regions with lower atlas-derived perfusion, regardless of the underlying diagnosis. These data suggest that across diverse disease processes, WM injury may occur in a pattern that reflects underlying tissue properties, such as relative perfusion.