g , Alzheimer’s disease, vascular dementia; Pakrasi and O’Brien 2

g., Alzheimer’s disease, vascular dementia; Pakrasi and O’Brien 2005; Austin et al. 2011) and has also been linked with more Bcr-Abl assay subtle deficits in nearly all domains of cognitive function in persons with cardiovascular disease (CVD; Jefferson et al. 2007a,b; Appleman et al. 2010; Moser et al. 2012). The inverse association between CBF and cognitive function likely stems from the adverse effects of cerebral hypoperfusion on the brain (Jefferson

et al. 2007a; Jerskey et al. 2009). Reduced CBF has been shown to predict decreased Inhibitors,research,lifescience,medical brain volume in persons with diabetes (van Elderen et al. 2011). Measures of systemic perfusion (e.g., cardiac indices) also significantly correlate with abnormal brain aging (e.g., smaller brain volume, white matter hyperintensities [WMH]) in patients with cardiac disease (Jefferson et al. 2007b, 2010; Jefferson 2010). Extant evidence also shows that reduced CBF is associated with structural and functional brain abnormalities in a wide range of medical and neurological populations (e.g., Alzheimer’s disease, stroke patients; Inhibitors,research,lifescience,medical Austin et al. 2011; Aoi et al. 2012). Despite these findings, the independent effects of cerebral perfusion on cognitive function and brain structure remains poorly understood. Inhibitors,research,lifescience,medical Recent studies have used positron emission tomography (PET) and found global CBF was inversely associated with cognitive test performance among vascular disease patients; however, findings from these

studies are limited by small sample sizes and lack of control for confounding comorbid medical conditions that influence neurocognitive outcomes (Kitagawa et al. 2009; Brundel Inhibitors,research,lifescience,medical et

al. 2012; Moser et al. 2012). Even further, limited research has used arterial spin labeling (ASL) to examine the relationship between CBF and neurocognitive outcomes in aging older adults with CVD. This is unfortunate, as rapidly growing attention has been paid to the use of ASL imaging in detecting individuals at risk for neurodegenerative disorders (e.g., Alzheimer’s disease), including conversion from normal aging to dementia (Chao et al. 2010; Alexopoulos et al. 2012; Inhibitors,research,lifescience,medical Bangen et al. 2012; Wolk and Detre 2012). Past work also shows ASL imaging is sensitive to brain perfusion abnormalities in stroke mafosfamide survivors even before the onset of structural brain injury – though this study was limited to sample size of three participants (Brumm et al. 2010). In light of these findings, ASL imaging may also serve as a useful biomarker for poor neurocognitive outcomes in aging older adults with CVD at risk for cognitive impairment, though no study has examined this possibility. The purpose of the current study was to examine the independent associations among cerebral perfusion using ASL imaging, structural brain indices (e.g., volume and cortical thickness), and cognitive test performance among a larger sample of older adults with varying degrees of vascular disease.

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