Global and executive cognitive functions predict declines in gait speed. The association of ECF with gait speed decline is attenuated by comorbid conditions, particularly depression. Elucidation of the mechanisms underlying these associations may point to new pathways for the treatment of physical decline associated with diminished cognitive function.

In this well-functioning cohort, several cognitive tasks were associated with gait speed cross-sectionally and predicted longitudinal gait speed decline. These data are consistent with a shared pathology underlying cognitive and motor declines but do not suggest that specific executive cognitive deficits account for slowing of usual gait in aging.

Background Hypertension (HTN) is a risk factor for dementia and animal studies suggest that centrally active (cross the blood brain barrier) angiotensin converting enzyme (ACE) inhibitors may protect against dementia beyond HTN control. Methods Participants in the Cardiovascular Health Study cognition substudy (mean age 75 yrs) with treated HTN and no diagnosis of heart failure (n= 1054) were followed for a median of 6 years to determine whether cumulative exposure to ACE inhibitors (as a class and by central activity), compared to other antihypertensive agents, was associated with lower risk of incident dementia, cognitive decline (by the modified mini mental state exam, 3MSE), or incident disability in instrumental activities of daily living (IADL). Results Among 414 participants exposed to ACE inhibitors and 640 not, there were 158 cases of incident dementia. Compared to other anti-HTN drugs, there was no association between exposure to all ACE inhibitors and risk of dementia (HR 1.01, 95% CI 0.88–1.15), difference in 3MSE scores (−0.32 points/yr, p=0.15), or odds of IADL disability (OR (95% CI) 1.06 (0.99–1.14). Adjusted results were similar. However, centrally active ACE inhibitors were associated with 65% less decline in 3MSE scores per year of exposure (p= 0.01) and non-centrally active ACE inhibitors were associated with greater risk of incident dementia (adjusted HR 1.20 (1.00–1.43) per year of exposure) and greater odds of IADL disability (adjusted OR 1.16 (1.03–1.30) per year of exposure) compared to other anti-HTN drugs. Conclusions While ACE inhibitors as a class do not appear to be independently associated with dementia risk or cognitive decline in older hypertensive adults, there may be within class differences in regards to these outcomes. These results should be confirmed with an RCT of a centrally active ACE inhibitor in the prevention of cognitive decline and dementia.

Background: Age-related body-composition changes are associated with health-related outcomes in elders. This relation may be explained by inflammation and hemostatic abnormalities. Objectives: Our objectives were to evaluate the relation between body-composition measures [body mass index (BMI), total fat mass, and appendicular lean mass (aLM)] and C-reactive protein (CRP), interleukin 6 (IL-6), and plasminogen activator inhibitor 1 (PAI-1) and to explore the effect of obesity and sarcopenia on CRP, IL-6, and PAI-1 concentrations. Design: The data are from the Trial of Angiotensin Converting Enzyme Inhibition and Novel Cardiovascular Risk Factors (TRAIN) study baseline visit (n ҃ 286; mean age ҃ 66.0 y). Total fat mass and aLM were assessed with a dual-energy X-ray absorptiometry scan. Linear regressions were performed between body-composition measures and CRP, IL-6, or PAI-1 concentrations. The effect of sarcopenia and obesity (defined as the percentage of fat mass) on CRP, IL-6, and PAI-1 concentrations was evaluated with the use of analyses of covariance. Results: CRP and IL-6 were positively associated with both BMI [␤ ҃ 0.027 (P ҃ 0.03) and ␤ ҃ 0.048 (P 0.001), respectively] and total fat mass [␤ ҃ 0.049 (P 0.001) and ␤ ҃ 0.055 (P 0.001), respectively] and were inversely associated with fat-adjusted aLM [␤ ҃ Ҁ0.629 (P ҃ 0.002) and ␤ ҃ Ҁ0.467 (P ҃ 0.02), respectively]. PAI-1 was positively associated with both BMI (␤ ҃ 0.038, P ҃ 0.005) and total fat mass (␤ ҃ 0.032, P ҃ 0.007). No significant interaction was found between either obesity or sarcopenia and CRP, IL-6, and PAI-1 concentrations. Obesity remained significantly associated with high CRP and IL-6 concentrations after adjustments for sarcopenia. Conclusions: CRP and IL-6 are positively associated with total fat mass and negatively associated with aLM. Obesity-associated inflammation may play an important role in the age-related process that leads to sarcopenia. The relation of inflammation with sarcopenia was not independent of any of the considered obesity indexes.Am J Clin Nutr 2005;82:428 -34.