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Background Half of all physical disability, including activity of daily living (ADL) disability, among older adults occurs in the setting of hospitalization. This study examines whether appendicular lean mass (ALM) and grip strength, which are commonly included in various definitions of sarcopenia, are associated with the development of hospital-associated ADL disability in older adults in the Health ABC Study. Methods Individuals hospitalized during the first 5 years of follow-up (n = 1 724) were analyzed. ALM to body mass index (BMI) ratio (ALMBMI), by dual-energy x-ray absorptiometry (DXA), and grip strength, by hand-held dynamometery, were assessed annually. Development of new ADL disability was assessed at the time of the next annual assessment after hospitalization. Separate regression analyses modeled the association of prehospitalization ALMBMI or grip strength with death before the next scheduled annual assessment. Next, among those who survived to the next annual assessment, separate regression analyses modeled the association of ALMBMI or grip strength with development of ADL disability. Results Each standard deviation decrement in prehospitalization grip strength was associated with an adjusted 1.80 odds of new ADL disability at follow-up (95% CI: 1.18, 2.74). Low, compared with not low, grip strength (per FNIH definition) was associated with an adjusted 2.36 odds of ADL disability at follow-up (95% CI: 1.12, 4.97). ALM measures were not associated with the development of hospital-associated ADL disability. ALM and grip strength measures were not associated with death. Conclusions Prehospitalization lower grip strength may be an important risk factor for ADL disability among older adult survivors of hospitalization.

Objectives Better understanding of the lifestyle activities shared among older adult subgroups may inform further health behavioral interventions that can be deployed at the group or community level. We applied latent class analysis to characterize qualitatively distinct lifestyle engagement groups, examined their differential risk of incident dementia, and compared their predictive utility to traditional activity frequency and variety scores. Method Participants were from the Ginkgo Evaluation of Memory Study (N = 3,068, mean age = 78.5). Lifestyle activities were measured at baseline using the Lifestyle Activity Questionnaire. All-cause dementia was screened every 6 months and cases were clinically adjudicated. Median follow-up was 6 years. Time to dementia was assessed using discrete-time proportional hazards models, adjusted for demographic and health covariates. Results Latent classes provided slightly poorer case discrimination than the frequency scores but identified distinct qualitative subgroups. In the 4-class model, the Variety (22%) and Intellectual (18%) lifestyle groups had high engagement in intellectual activities, whereas the Variety and Social groups (32%) had high engagement in formal social activities. Compared to the Least Active group (28%), the Variety (hazard ratio [HR] = 0.67, 95% confidence interval [CI]: 0.48, 0.93) and Intellectual (HR = 0.65, 95% CI: 0.45, 0.93) groups had significantly lower risk of incident dementia, but only among those without prevalent mild cognitive impairment. Discussion Older adults highly engaged in intellectual activities, but not necessarily social activities, had the lowest risk of incident dementia. Activity frequency scores provided only slightly better case discrimination than activity variety scores and latent classes. Latent classes of older adults differed by their amount and types of activities, which may inform intervention design.

BACKGROUND The importance of systemic inflammation, measured by C-reactive protein, in cognitive decline has been demonstrated; however, the role of vascular inflammation is less understood. Pentraxin 3 (PTX3) is a novel marker of vascular inflammation. METHODS We followed adults 65 and older, free of cardiovascular disease (CVD) for up to 9 years (n = 1,547) in the Cardiovascular Health Study. We evaluated the relationship between PTX3 and change in cognitive function, measured using the Modified Mini-Mental State Examination (3MSE), and incident cognitive impairment (3MSE < 80). Mediation by CVD events, and effect modification by sex and apolipoprotein E ɛ4 allele (APOE4) were also examined. RESULTS The average decline in 3MSE was 0.77 points per year. The association between PTX3 and change in 3MSE differed between women and men (p = .02). In the adjusted model, each standard deviation higher in PTX3 was associated with a 0.20 greater decline in 3MSE score per year in women over follow-up (95% CI: -0. 37, -0.03; p = .02), compared to no change in men (β = 0.07; 95% CI: -0.08, 0.22). CVD events had a minor effect on the associations. No effect modification by APOE4 was found, although we observed the association of PTX3 and cognitive impairment in women was attenuated and nonsignificant after adjustment for APOE4. There was a paradoxical protective association between PTX3 and reduced cognitive impairment in men, even after adjustment for APOE4. CONCLUSIONS We found that vascular inflammation was significantly associated with cognitive decline in older women, but not men.

Background Vascular risk factors, including inflammation, may contribute to dementia development. We investigated the associations between peripheral inflammatory biomarkers and cognitive decline in five domains (memory, construction, language, psychomotor speed, and executive function). Methods Community-dwelling older adults from the Ginkgo Evaluation of Memory Study (n = 1,159, aged 75 or older) free of dementia at baseline were included and followed for up to 7 years. Ten biomarkers were measured at baseline representing different sources of inflammation: vascular inflammation (pentraxin 3 and serum amyloid P), endothelial function (endothelin-1), metabolic function (adiponectin, resistin, and plasminogen activating inhibitor-1), oxidative stress (receptor for advanced glycation end products), and general inflammation (interleukin-6, interleukin-2, and interleukin-10). A combined z-score was created from these biomarkers to represent total inflammation across these sources. We utilized generalized estimating equations that included an interaction term between z-scores and time to assess effect of inflammation on cognitive decline, adjusting for demographics (such as age, race/ethnicity, and sex), cardiovascular risk factors, and apolipoprotein E e4 carrier status. A Bonferroni-adjusted significance level of .01 was used. We explored associations between individual biomarkers and cognitive decline without adjustment for multiplicity. Results The combined inflammation z-score was significantly associated with memory and psychomotor speed (p < .01). Pentraxin 3, serum amyloid P, endothelin-1, and interleukin-2 were associated with change in at least one cognitive domain (p < .05). Conclusion Our results suggest that total inflammation is associated with memory and psychomotor speed. In particular, systemic inflammation, vascular inflammation, and altered endothelial function may play roles in domain-specific cognitive decline of nondemented individuals.

Although biologic age may be impossible to define completely, it will be better understood by uncovering biomarkers of aging. In the future, these biomarkers might guide preventive or therapeutic interventions before clinical onset of age-related disease. Leukocyte telomere length (LTL) might be such a biomarker because it ostensibly records the accruing burden of inflammation and oxidative stress, processes thought to contribute to aging and disease pathogenesis (1–3). LTL undergoes progressive shortening with age, and in the general population, it is comparatively short in individuals with atherosclerosis or those at risk for this aging-related disease (4). The evidence for LTL as an overall biomarker of aging remains unclear, though, due to variation in the strength of detected associations, differences in results based on measurement method and selected outcome, lack of data coupling longitudinal measurements of LTL and aging phenotypes, and theoretical considerations of whether a single marker can accurately and strongly record aging across the life span (5–7). Most studies of LTL concern only clinically diagnosed disease, but in cohort studies of older individuals without clinically diagnosed disease, the prevalence and severity range of subclinical disease can be substantial when assessed using several noninvasive methods (8–11). Furthermore, undiagnosed disease can powerfully predict incident adverse events independent of diagnosed disease (8–14). Defining disease in categorical (yes/no) terms is imprecise, whereas using quantitative biomarkers might provide a more realistic picture of age-related disease load. Therefore, previous studies relying on disease categorization may have missed associations between LTL and age-related disease. Most studies exploring the links between LTL and age-related disease have focused on a single organ or biologic system rather than “disease burden” across systems. Here, we define “disease burden” as the sum of noninvasively measured markers of age-related dysfunctions in structure or physiology of different organ systems. This distinction is relevant because LTL apparently records systemic burden of inflammation and oxidative stress. Thus, a study of LTL and disease burden is warranted to clarify the validity of LTL as a biomarker of aging or age-related disease. Recently, Newman and colleagues (15) developed a physiologic index of comorbidity (index), a 10-point scale that tabulates the severity of age-related chronic disease using noninvasive tests of the vasculature, lungs, kidneys, brain, and glucose metabolism. This estimates an individual’s disease burden regardless of whether disease is clinically recognized. Given its more continuous range, it demonstrated the spectrum of chronic disease in a general population of community-dwelling older adults. The index explained 40% of the age effect on mortality risk and illustrated that high disease burden, even when clinically unrecognized, was significantly associated with mobility limitation and failure to complete activities of daily living. The index appears to be a valid measure of disease burden and stratifies individuals into a wide range of risk. Using data on LTL and age-related disease burden from the Cardiovascular Health Study (CHS), we conducted this analysis to test two hypotheses: (a) Shorter LTL is associated with greater age-related disease burden and (b) shorter LTL is less strongly associated with disease in individual systems or diagnosed chronic conditions (cardiovascular disease, stroke, pulmonary disease, diabetes, kidney disease, arthritis, or depression).

MORE than one third of adults aged 65 years and older fall every year (1–3); this proportion increases with age (4). Falls have serious consequences in the elderly population, including injury (2,3), fear of falling again (5), depression (5), admission to a long-term care facility (6), and death (7). Approximately, 5% of all falls result in a serious injury (2,3), leading to substantial medical costs (8). The number of injuries and medical costs associated with falling will likely increase as the U.S. population ages. Identifying risk factors for falls in the elderly has long been of interest to researchers and clinicians intent on reducing morbidity and mortality in this age group. Impaired cognition is a risk factor for recurrent falls (9,10), injurious falls (11,12), and serious falls requiring hospitalization (13,14). There is also a strong relationship between falls, cognition, and physical function. Complex measures of physical function can predict cognitive decline (15) and falls (16) in healthy older adults. Specifically, low scores on tests of speed and executive function, including the Digit Symbol Substitution Test (DSST), are associated with increased risk of a fall (17). Incident stroke is associated with a subsequent decrease in cognition (18); many older adults with mild cognitive impairment also present with gait dysfunction (19). However, it is unknown whether decreased cognition, above the threshold of impairment, is also a risk factor for serious falls. Identifying a relationship between increasing levels of impairment in global cognition or specific cognitive domains may help to identify elderly subpopulations most at risk for serious falls. The objective of this study was to determine if decreased global cognitive function, processing speed, or both, as measured by standardized cognitive tests, are associated with increased risk of serious falls resulting in hospitalization in older adults. Hospitalization and study records from the Cardiovascular Health Study (CHS), a large longitudinal study population with 15 years of follow-up, were used to examine this association.