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Articles by Hugh C. Hendrie
Total Records ( 3 ) for Hugh C. Hendrie
  Kathleen S. Hall , Sujuan Gao , Olusegun Baiyewu , Kathleen A. Lane , Oye Gureje , Jianzhao Shen , Adesola Ogunniyi , Jill R. Murrell , Frederick W. Unverzagt , Jeanne Dickens , Valerie Smith- Gamble and Hugh C. Hendrie
  Background This study compares age-specific and overall prevalence rates for dementia and Alzheimer's disease (AD) in two nonoverlapping, population-based cohorts of elderly African Americans in Indianapolis in 2001 and 1992. Methods We used a two-stage design. The first stage involves the Community Screening Interview for Dementia (CSI-D). The CSI-D scores are grouped into good, intermediate, and poor performance before selection for clinical assessment. Diagnoses were performed using standard criteria in a consensus diagnosis conference; clinicians were blind to performance groups. In 1992, interviewers visited randomly sampled addresses to enroll self-identified African Americans aged ≥65 years. Of 2582 eligible, 2212 enrolled (9.6% refused, and 4.7% were too sick). In 2001, Medicare rolls were used for African Americans aged >70 years. Of 4260 eligible, 1892 (44%) enrolled, 1999 (47%) refused, and the remainder did not participate for other reasons. Results The overall age-adjusted prevalence rate for dementia at age ≥70 years in 2001 was 7.45% (95 confidence interval [CI], 4.27–10.64), and in the 1992 cohort, this prevalence rate was 6.75% (95% CI, 5.77–7.74). The overall age-adjusted prevalence rate at age ≥70 years for AD in the 2001 cohort was 6.77% (95% CI, 3.65–9.90), and for the 1992 cohort, it was 5.47% (95% CI, 4.51–6.42). Rates for dementia and AD were not significantly different in the two cohorts (dementia, P = .3534; AD, P = .2649). Conclusions We found no differences in the prevalence rates of dementia and AD between 1992 and 2001, despite significant differences in medical history and medical treatment within these population-based cohorts of African American elderly.
  Richard Mayeux , Christiane Reitz , Adam M. Brickman , Mary N. Haan , Jennifer J. Manly , M. Maria Glymour , Christopher C. Weiss , Kristine Yaffe , Laura Middleton , Hugh C. Hendrie , Lauren H. Warren , Kathleen M. Hayden , Kathleen A. Welsh- Bohmer , John C.S. Breitner and John C. Morris
  In this article, the challenges faced by several noted population studies for Alzheimer dementia in operationalizing current clinical diagnostic criteria for Alzheimer‘s disease (AD) have been reviewed. Differences in case ascertainment, methodological biases, cultural and educational influences on test performance, inclusion of special populations such as underrepresented minorities and the oldest old, and detection of the earliest symptomatic stages of underlying AD have been considered. Classification of Alzheimer dementia may be improved by the incorporation of biomarkers for AD if the sensitivity, specificity, and predictive value of the biomarkers are established and if they are appropriate for epidemiological studies, as may occur should a plasma biomarker be developed. Biomarkers for AD could also facilitate studies of the interactions of various forms of neurodegenerative disorders with cerebrovascular disease, resulting in ”mixed dementia“.
  Alette M. Wessels , Kathleen A. Lane , Sujuan Gao , Kathleen S. Hall , Frederick W. Unverzagt and Hugh C. Hendrie
  Background Diabetes mellitus is associated with an increased risk for cognitive impairment and vascular factors seem to play a role in this relationship. In a sample involving elderly African Americans, we tested the hypothesis that diabetes accelerates cognitive decline and explored possible mediating mechanisms within a follow-up period of 15 years. Methods A total of 1702 subjects, of whom 441 had diabetes, were given the community screening interview for dementia to measure cognitive functioning at six different time points spread over a 15-year follow-up period. Mixed effects models with repeated measures were used to examine the association of diabetes and vascular risk factors with cognitive scores over time. Results African American subjects with diabetes reported having a significant accelerated cognitive decline as compared with those without diabetes (P = .046), when controlling for basic demographics and baseline comorbid conditions (heart disease, hypertension, stroke, and depression). Adjusting for incident heart disease, and especially stroke, weakened this association (P = .098), thereby indicating a mediating effect of stroke on the association between diabetes and cognitive decline. However, when incident stroke was incorporated into the model, the effect for participants with diabetes increased greatly (P = .007). Conclusions Diabetes, mediated by cerebrovascular pathology, accelerates cognitive decline within a follow-up period of 15 years in a sample comprising African Americans.
 
 
 
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