Search

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]

OBJECTIVES: To assess the longitudinal association between sleep disturbances (insomnia and daytime sleepiness) and incidence of dementia and cognitive decline in older men. DESIGN: Community-based longitudinal cohort study. SETTING: The Honolulu-Asia Aging Study of dementia that is linked to the Honolulu Heart Program's fourth examination, conducted 1991–1993, and the 3-year follow-up fifth examination, conducted 1994–1996. PARTICIPANTS: Two thousand three hundred forty-six Japanese-American men age 71 to 93 years who screened negative for prevalent dementia at baseline and were screened again for dementia incidence in a 3-year follow-up examination. MEASUREMENTS: Baseline self-reports of trouble falling asleep or early morning awakening (insomnia) and being sleepy during the day (daytime sleepiness); Cognitive Abilities Screening Instrument (CASI) scores from baseline and followup; clinical diagnosis of incident dementia; and other baseline measures including age, years of education, body mass index, depressive symptoms, and history of hypertension, heart disease, diabetes mellitus, asthma, and use of benzodiazepines. RESULTS: After adjusting for age and other factors, persons reporting excessive daytime sleepiness at baseline (8%) were twice as likely to be diagnosed with incident dementia than were those not reporting daytime sleepiness (odds ratio (OR) = 2.19, 95% confidence interval (CI) = 1.37–3.50) and about 40% more likely to have ≥9 point drop in their CASI score between examinations (OR = 1.44, 95% CI = 1.01–2.08). In contrast, insomnia was not associated with cognitive decline or incidence of dementia. CONCLUSIONS: Daytime sleepiness in older adults may be an early indicator of decline in cognitive functioning and onset of dementia. [ABSTRACT FROM AUTHOR]

Background The timed 10-foot walk is used clinically to diagnose and monitor functional impairment. Case-control studies have shown slower walking speeds in patients with prevalent Parkinson's disease (PD). We examined whether walking time predicts 10-year incident PD in elderly Japanese-American men. Methods The Honolulu-Asia Aging Study began with the fourth Honolulu Heart Program examination in 1991-93, when 3606 Japanese- American men ages 71-93 years performed the timed 10-foot walk. Walking time (seconds) was used both as a continuous variable and divided into three groups (fast, intermediate, slow). Subgroup analysis excluded those with prevalent stroke or dementia at baseline. Both prevalent (n = 66) and incident (n = 45) PD were studied as outcomes. Final diagnosis of PD was based on consensus from 2 neurologists using standardized criteria. Chi-square tests, T-tests, multiple logistic regression and Cox regression were used for analyses. This study was approved by the IRB of Kuakini Medical Center. Results The prevalence of PD was highest in those with slowest walking times (3.1%, 1.2%, 0.4% respectively, p <0.0001). Using multiple logistic regression analyses adjusting for age, triceps skinfold thickness, midlife smoking and midlife caffeine, those with the slowest (OR = 7.39, 95% CI = 2.92-18.73, p <0.0001) and intermediate (OR = 2.88, 95% CI = 1.10-7.57, p = 0.03) walking times were significantly more likely to have prevalent PD compared to those with the fastest walk times (reference). Cox proportional hazards models demonstrated a significant increase in risk of 10-year incident PD in those with slow walk times compared to fast (RR = 2.26, 95% CI = 1.08-4.73, p = 0.03). This relationship was slightly stronger when subjects with prevalent stroke or dementia at baseline were excluded (RR = 2.49, CI = 1.19-5.21, p = 0.02). Conclusion Slower walk time was significantly independently associated with prevalent PD, and with 10-year incident PD. It is likely that slow walking time is a marker of pre-clinical PD, in addition to being a manifestation of clinically recognized PD. Early screening for PD will be helpful when treatments become available that delay or arrest progression of disease. [ABSTRACT FROM AUTHOR]

Background There are many variations of the Circle of Willis (COW). The purpose of this study was to compare the prevalence at autopsy of hypoplasticity of the posterior communicating artery (PCoA) in Japanese American men to results from studies involving other ethnic groups. Methods 703 men of the Honolulu Asia-Aging Study (HAAS) were autopsied and the COW was dissected and examined. Hypoplasticity of the PCoA was recorded and compared with previous studies. Results The prevalence of hypoplastic PCoA was found to be greater in HAAS men than in other published reports. Previous studies reported hypoplasia of the PCoA ranging from 16.7% - 81% of cases. In this series, some degree of PCoA hypoplasia was observed in 85% of decedents, including 60.2% with bilateral hypoplasia. The age at death was unassociated with the severity, side, uni-laterality or bilaterality of the hypoplasia. Conclusion A high prevalence of hypoplastic PCoA was observed in this cohort. The lack of any apparent relationship with age at death suggests that brain perfusion sufficient to sustain life was not embarassed by the hypoplasia. Additional analyses will be needed to address the likely origins of the hypoplasia, and to discern any impact on parenchymal brain structure, or relationship with infarcts, hemorrhages, or atrophy. [ABSTRACT FROM AUTHOR]