This study provides evidence that performance measures can validly characterize older persons across a broad spectrum of lower extremity function. Performance and self-report measures may complement each other in providing useful information about functional status.
Objectives: To provide updated estimates of Alzheimer disease (AD) dementia prevalence in the United States from 2010 through 2050.Methods: Probabilities of AD dementia incidence were calculated from a longitudinal, populationbased study including substantial numbers of both black and white participants. Incidence probabilities for single year of age, race, and level of education were calculated using weighted logistic regression and AD dementia diagnosis from 2,577 detailed clinical evaluations of 1,913 people obtained from stratified random samples of previously disease-free individuals in a population of 10,800. These were combined with US mortality, education, and new US Census Bureau estimates of current and future population to estimate current and future numbers of people with AD dementia in the United States.Results: We estimated that in 2010, there were 4.7 million individuals aged 65 years or older with AD dementia (95% confidence interval [CI] 5 4.0-5.5). Of these, 0.7 million (95% CI 5 0.4-0.9) were between 65 and 74 years, 2.3 million were between 75 and 84 years (95% CI 5 1.7-2.9), and 1.8 million were 85 years or older (95% CI 5 1.4-2.2). The total number of people with AD dementia in 2050 is projected to be 13.8 million, with 7.0 million aged 85 years or older.
Conclusion:
GROWING BODY OF EVIDENCE suggests that oxidative processes may be involved in the etiology of Alzheimer disease (AD). 1 Accumulated damage to lipid membranes and DNA by oxygen free radicals and reactive oxygen species is thought to disrupt normal cell functioning and lead to neuronal death. 2 Antioxidant nutrients, including vitamin E, vitamin C, and beta carotene, are among the body's natural defense mechanisms against oxidative stress. The antioxidant nutrients have been shown through animal and laboratory studies of brain tissue to decrease lipid peroxidation 3-11 and the oxidation of proteins, 12,13 inhibit the production of reactive oxygen species, 6,14,15 prevent mitochondrial dysfunction 12,16 and DNA fragmentation, 6,17 and reduce neurotoxicity, 18,19 apoptosis, 15,19-21 and neuronal death. 18,22 Few studies have examined the relation between dietary intake of antioxidant nutrients and the development of AD. Two prospective studies 23,24 that reported on the association of vitamin E and vitamin C supplement use and AD yielded conflicting results, but both had limited power to test the hypothesis, and neither had dietary information. We report on the association between incident AD and intake of antioxidant nutrients from foods and supplements in a large community study, the Chicago Health and Aging Project (CHAP).
Two brief screening tests, the Short Portable Mental Status Questionnaire (SPMSQ) and the East Boston Memory Test (EBMT), were included in a population questionnaire administered to 3,811 persons 65 years of age and older. A detailed clinical evaluation was then administered to 467 persons (drawn from high, medium and low performers on the EBMT) to determine who was cognitively impaired and the disorders that were responsible for that cognitive impairment. The results showed that the EBMT was better at enriching the population of the poor performance group with persons who had Alzheimer's disease (AD). It had a lower refusal rate among non-proxy respondents: 2% for the EMBT versus 9% for the SPMSQ. The sensitivity and positive predictive value were also higher for the EBMT than the SPMSQ when the diagnosis of interest was AD. However, there were persons with AD in all strata of performance on both the EBMT and the SPMSQ, emphasizing the importance of selecting persons from all performance strata in multistage community studies of AD.
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