https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41204 Thu 28 Jul 2022 11:26:39 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22411 Thu 22 Sep 2016 10:55:42 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32314 Mon 23 Sep 2019 12:52:02 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38215 50 years, n = 92). The latter were further subdivided into two subgroups with (CV+, n = 25) and without (CV−, n = 67) cardiovascular risk factors. Arterial pulsatility was measured using cardiac-gated phase-contrast flow quantification sequence and three indexes of whole-brain white matter microstructural organization [i.e., fractional anisotropy (FA), radial diffusivity (RaD), mean diffusivity (MD)] were derived from diffusion-weighted imaging (DWI). Cognitive ability was assessed using global cognitive functioning (MoCA) and a measure of working memory [sensitivity (d′) from a 2-back task]. Neither the whole group analysis nor the younger adult group showed an association between measures of arterial pulsatility, global white matter microstructural organization, and cognition. In older adults, higher MD and RaD were associated with increased arterial pulsatility and poorer working memory performance. The indirect pathway from arterial pulsatility to working memory performance via both MD and RaD measures was significant in this group. Interestingly, a comparison of CV+ and CV− subgroups showed that this mediating relationship was only evident in older adults with at least one CV risk factor. These findings are consistent with cardiovascular risk factors as underlying arterial, white matter, and cognitive decline in cognitively normal older adults.]]> Fri 13 Aug 2021 14:31:48 AEST ]]>