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Background: This study aimed to investigate the factors associated with the time that community-dwelling stroke survivors spent walking. Methods: We analyzed the cross-sectional data of 1534 community-dwelling stroke survivors from the Korean National Health and Nutrition Examination Survey. Complex-sample logistic regression analyses were performed to determine the factors associated with insufficient walking time (<90 min/wk). The mean time spent walking was examined according to age, sex, resistance exercise level, and self-reported disability using complex-sample general linear models. Results: Women (odds ratio [OR] 1.5; 95% confidence interval [CI], 1.0–2.3), current smokers (OR 1.7; 95% CI, 1.1–2.8), insufficient resistance exercise (OR 2.3; 95% CI, 1.5–3.5), and those with rural residences (OR 1.4; 95% CI, 1.0–1.9) were independently associated with insufficient walking time. The mean time spent walking was significantly lower in older adults aged ≥65 years than in young adults aged <65 years (200.0 ± 42.0 min/wk vs 287.2 ± 36.6 min/wk, P =.002), in women than in men (200.9 ± 44.9 vs 286.2 ± 37.7 min/wk, P =.027), and in individuals engaging in insufficient resistance exercise compared with those engaging in sufficient resistance exercise (203.2 ± 36.2 vs 283.9 ± 43.0 min/wk, P =.008). The mean walking time did not vary according to the presence of self-reported disabilities. Conclusions: Environmental and personal factors are associated with insufficient walking time in community-dwelling stroke survivors. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) survivors face debilitating long-term psychosocial consequences, including social isolation and depression. TBI modifies neurovascular physiology and behavior but the chronic physiological implications of altered brain perfusion on social interactions are unknown. Adult C57/BL6 male mice received a moderate cortical TBI, and social behaviors were assessed at baseline, 3-, 7-, 14-, 30-, and 60-days post injury (dpi). Magnetic resonance imaging (MRI, 9.4T) using dynamic susceptibility contrast perfusion weighted MRI were acquired. At 60dpi mice underwent histological angioarchitectural mapping. Analysis utilized standardized protocols followed by cross-correlation metrics. Social behavior deficits at 60dpi emerged as reduced interactions with a familiar cage-mate (partner) that mirrored significant reductions in cerebral blood flow (CBF) at 60dpi. CBF perturbations were dynamic temporally and across brain regions including regions known to regulate social behavior such as hippocampus, hypothalamus, and rhinal cortex. Social isolation in TBI-mice emerged with a significant decline in preference to spend time with a cage mate. Cortical vascular density was also reduced corroborating the decline in brain perfusion and social interactions. Thus, the late emergence of social interaction deficits mirrored the reduced vascular density and CBF in regions known to be involved in social behaviors. Vascular morphology and function improved prior to the late decrements in social function and our correlations strongly implicate a linkage between vascular density, cerebral perfusion, and social interactions. Our study provides a clinically relevant timeline of alterations in social deficits alongside functional vascular recovery that can guide future therapeutics.

Adults with Down syndrome have a genetic form of Alzheimer's disease (AD) and evidence of cerebrovascular disease across the AD continuum, despite few systemic vascular risk factors. The onset and progression of AD in Down syndrome is highly age-dependent, but it is unknown at what age cerebrovascular disease emerges and what factors influence its severity. In the Alzheimer's Biomarker Consortium-Down Syndrome study (ABC-DS; n = 242; age = 25-72), we estimated the age inflection point at which MRI-based white matter hyperintensities (WMH), enlarged perivascular spaces (PVS), microbleeds, and infarcts emerge in relation to demographic data, risk factors, amyloid and tau, and AD diagnosis. Enlarged PVS and infarcts appear to develop in the early 30s, while microbleeds, WMH, amyloid, and tau emerge in the mid to late 30s. Age-residualized WMH were higher in women, in individuals with dementia, and with lower body mass index. Participants with hypertension and APOE-ε4 had higher age-residualized PVS and microbleeds, respectively. Lifespan trajectories demonstrate a dramatic cerebrovascular profile in adults with Down syndrome that appears to evolve developmentally in parallel with AD pathophysiology approximately two decades prior to dementia symptoms.