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The authors examined whether low levels of social engagement in midlife and late life were associated with the risk of incident dementia in 2,513 Japanese-American men who have been followed since 1965 as part of the Honolulu Heart Program and the Honolulu-Asia Aging Study. In 1991, assessment of dementia began; incident dementia cases (n = 222) were diagnosed in 1994 and 1997. Social engagement was assessed in midlife (1968) and late life (1991). The relation between social engagement and dementia risk was examined using Cox proportional hazards models. No level of midlife social engagement was associated with the risk of dementia. In late life, compared with participants in the highest quartile of late-life social engagement, those in the lowest quartile had a significantly increased risk of dementia (hazard ratio = 2.34, 95% confidence interval: 1.18, 4.65). However, compared with those who were in the highest quartile of social engagement at both midlife and late life, only decreased social engagement from midlife to late life was associated with an increased risk of dementia (hazard ratio = 1.87, 95% confidence interval: 1.12, 3.13). Although low social engagement in late life is associated with risk of dementia, levels of late-life social engagement may already have been modified by the dementing process and may be associated with prodromal dementia. [ABSTRACT FROM AUTHOR]

Dementia, Alzheimer's disease in particular, is one of the major causes of disability and decreased quality of life among the elderly and a leading obstacle to successful aging. Given the profound impact on public health, much research has focused on the age-specific risk of developing dementia and the impact on survival. Early work has discussed various methods of estimating age-specific incidence of dementia, among which the illness-death model is popular for modeling disease progression. In this article we use multiple imputation to fit multi-state models for survival data with interval censoring and left truncation. This approach allows semi-Markov models in which survival after dementia depends on onset age. Such models can be used to estimate the cumulative risk of developing dementia in the presence of the competing risk of dementia-free death. Simulations are carried out to examine the performance of the proposed method. Data from the Honolulu Asia Aging Study are analyzed to estimate the age-specific and cumulative risks of dementia and to examine the effect of major risk factors on dementia onset and death.

The association between apolipoproteins and neurodegeneration is unclear. The authors examined the association of dementia with serum levels of apolipoprotein A-I (ApoA-I) alone and in combination with the apolipoprotein E genotype (ApoE). Subjects were Japanese-American men in Hawaii followed since 1965 in the Honolulu Heart Program cohort and the Honolulu-Asia Aging Study. Lipid levels were assessed in 1980-1982. Dementia was diagnosed in 1991-1993, 1994-1996, and 1997-1999 by using a multistep procedure and international guidelines. The sample consisted of 929 men (107 dementia cases). The relation between ApoA-I and dementia was examined by using Cox proportional hazards models adjusted for age, education, and cardiovascular risk factors. Compared with men in the lowest quartile, men in the highest quartile of ApoA-I concentration had a significantly lower risk of dementia (hazard ratio = 0.25, 95% confidence interval: 0.08, 0.78). Compared with men with both risk factors, those with a high ApoA-I concentration and no ApoE epsilon4 had a significantly lower risk of dementia (hazard ratio = 0.21, 95% confidence interval: 0.08, 0.52). Previous work has demonstrated an inverse relation between ApoA-I and cardiovascular disease, and the authors extended these findings to the risk of dementia. These results raise the possibility that different lipoprotein components of cholesterol may be differentially associated with dementia.