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Arterial Spin-Labeling Parameters and Their Associations with Risk Factors, Cerebral Small-Vessel Disease, and Etiologic Subtypes of Cognitive Impairment and Dementia

Gyanwali, B.; Seng Tan, C.; Petr, J.; Tirado Escobosa, L. L.; Vrooman, H.; Chen, C.; Mutsaerts, H. J. M. M.; Hilal, S.


Background and purpose: Cerebral small vessel disease (SVD) may alter cerebral blood flow (CBF) leading to brain changes and hence cognitive impairment and dementia. CBF and spatial coefficient of variation (sCoV) can be measured quantitatively by Arterial Spin Labeling (ASL). We aim to investigate the associations of demographic, vascular risk factors, location and severity of SVD as well as etiologic subtypes of cognitive impairment and dementia with ASL parameters.
Methods: 390 patients; no cognitive impairment, cognitive impairment no dementia (CIND), vascular CIND (VCIND), Alzheimer’s disease (AD), and Vascular Dementia (VaD) were recruited from memory-clinic. Cerebral microbleeds (CMBs) and lacunes were categorized into strictly lobar, strictly deep, and mixed-location; enlarged perivascular spaces (ePVS) into centrum semiovale and basal ganglia. Total and region-specific white matter hyperintensity (WMH) volumes were segmented using FreeSurfer. CBF (n= 333) and sCoV (n=390) were analyzed with ExploreASL from 2D-EPI pseudo-continuous ASL-images.
Results: Increasing age, male sex, hypertension, hyperlipidemia, history of heart disease and smoking were associated with lower CBF and higher sCoV. Higher numbers of lacunes and CMBs were associated with lower CBF and higher sCoV. Location-specific analysis showed mixed-location lacunes and CMBs were associated with lower CBF. Higher total, anterior and posterior WMH volumes were associated with higher sCoV. No association was observed between ePVS and ASL parameters. Higher sCoV was associated with the diagnosis of VCIND, AD and VaD.
Conclusion: Reduced CBF and increased sCoV were associated with SVD, cognitive impairment, and dementia, suggesting that hypoperfusion might be the key underlying mechanism for vascular brain damage.

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