High-density Lipoprotein Cholesterol, Cognitive Function and Mortality in a U.S. National Cohort

Low levels of both high density lipoprotein cholesterol (HDL) and cognitive function are associated with increased mortality risk. HDL plays an important role in brain metabolism. We test the hypotheses that the relative protective effect of high HDL level as related to mortality is greater in persons with impaired cognitive function than in others. Data were analyzed from a longitudinal mortality follow-up study of 4911 American men and women aged 60 years and over examined in 1988-1994 followed an average 8.5 yr. Measurements at baseline included HDL, a short index of cognitive function (SICF), socio-demographics, health status, and self-reported leisure-time physical activity. In proportional hazards regression analysis, no significant interaction of HDL with cognitive function was found (p = 0.08); there was a significant age-SICF interaction. After stratifying by age and adjusting for confounding by multiple variables, independent associations of HDL and SICF score with survival were strongest among the oldest persons. Consistent with its association with HDL, cognitive function and survival, controlling in addition for physical activity reduced the associations. In a nationwide cohort of older Americans, analyses demonstrated a lower risk of death independent of confounders among those high HDL and SICF scores, strongest among the oldest persons

Population Surveillance of Dementia Mortality

Geographic and temporal variation in occurrence of dementia within the US has received little attention despite its importance for generation of new etiologic hypotheses and health services research. We examine methodological problems in the use of vital statistics data for assessing variation over time, among states and within states in the US. We analyzed the US multiple cause of death files for 2005–2006 and 1999–2000 US deaths with Alzheimer’s Disease (International Classification of Disease 10th revision code G30) and other dementias (codes F01, F02, R54) coded as underlying or contributing cause of death based on the death certificate. Age-adjusted death rates were computed by year, state or county for persons aged 65 years and over. In 2005–2006 combined, 555,904 total deaths occurred with any dementia type (212,386 for Alzheimer’s disease) coded as underlying or contributing cause. Among the states, age-adjusted rates per 100,000 per year varied by two fold ranging from 458 in New York to 921 in Oregon. Similar geographic patterns were seen for Alzheimer’s disease. However, between 1999–2000 and 2005–2006 the US death rate for all dementia increased only from 559 to 695 (24%) while that for Alzheimer’s disease doubled from 135 to 266. Use of specific (G30, F01) versus non-specific diagnoses (F02, R54) varied among states and over time, explaining most of the temporal increase in rate of Alzheimer’s disease. Further research is needed to assess artifacts of diagnosis, certification or coding, utilization of health services, versus biological variation as possible causes of temporal and geographic variation to enhance utility of mortality data for dementia monitoring and research

Correlates of serum lipoprotein (A) in children and adolescents in the United States. The third National Health Nutrition and Examination Survey (NHANES-III)

OBJECTIVE: To determine the correlates of serum lipoprotein (a) (Lp(a)) in children and adolescents in the United States. METHODS: Cross-sectional study using representative data from a US national sample for persons aged 4–19 years participating in The Third National Health Nutrition and Examination Survey (NHANES-III). RESULTS: We observed ethnicity-related differences in levels of Lp(a) > 30 mg/dl, with values being markedly higher in African American (black) than nonhispanic white (white) and Mexican American children in multivariate model (P < 0.001). Higher levels of Lp(a) > 30 mg/dl associated with parental history of body mass index and residence in metro compared to nonmetro in Blacks, and high birth weight in Mexican American children in the NHANES-III. In the entire group, total cholesterol (which included Lp(a)) and parental history of premature heart attack/angina before age 50 (P < 0.02) showed consistent, independent, positive association with Lp(a). In subgroup analysis, this association was only evident in white (P = 0.04) and black (P = 0.05) children. However, no such collective consistent associations of Lp(a) were found with age, gender, or birth weight. CONCLUSION: Ethnicity-related differences in mean Lp(a) exist among children and adolescents in the United States and parental history of premature heart attack/angina significantly associated with levels of Lp(a) in children. Further research on the associations of Lp(a) levels in childhood with subsequent risk of atherosclerosis is needed

Neuroprotection and Neurodegeneration in Alzheimer's Disease: Role of Cardiovascular Disease Risk Factors, Implications for Dementia Rates, and Prevention with Aerobic Exercise in African Americans

Prevalence of Alzheimer's disease (AD) will reach epidemic proportions in the United States and worldwide in the coming decades, and with substantially higher rates in African Americans (AAs) than in Whites. Older age, family history, low levels of education, and ɛ4 allele of the apolipoprotein E (APOE) gene are recognized risk factors for the neurodegeneration in AD and related disorders. In AAs, the contributions of APOE gene to AD risk continue to engender a considerable debate. In addition to the established role of cardiovascular disease (CVD) risk in vascular dementia, it is now believed that CVD risk and its endophenotype may directly comediate AD phenotype. Given the pleiotropic effects of APOE on CVD and AD risks, the higher rates of CVD risks in AAs than in Whites, it is likely that CVD risks contribute to the disproportionately higher rates of AD in AAs. Though the advantageous effects of aerobic exercise on cognition is increasingly recognized, this evidence is hardly definitive, and data on AAs is lacking. In this paper, we will discuss the roles of CVD risk factors in the development of AD and related dementias, the susceptibility of these risk factors to physiologic adaptation, and fitness-related improvements in cognitive function. Its relevance to AD prevention in AAs is emphasized

Smoking, Cognitive Function and Mortality in a U.S. National Cohort Study

Previous studies report that low levels cognitive function and history of smoking are associated with increased mortality risk. Elderly smokers may have increased risk of dementia, but risk in former smokers is unclear. We tested the hypotheses that the harmful effect of impaired cognitive function as related to mortality is greater in persons smoking at baseline than in others. Further, we used serum cotinine levels to assess recall bias of smoking history by cognitive function level. Data were analyzed from a longitudinal mortality follow-up study of 4,916 American men and women aged 60 years and over, examined in 1988–1994 with complete data followed an average 8.5 years. Measurements at baseline included smoking history, a short index of cognitive function (SICF), serum cotinine and socio-demographics. Death during follow-up occurred in 1,919 persons. In proportional hazards regression analysis, a significant interaction of current smoking with cognitive function was not found; but there was a significant age-smoking interaction. After adjusting for confounding by age or multiple variables, current smoking associated with over 2-fold increased mortality (hazards ratio and 95% confidence limits current versus never smoking 2.13, 1.75–2.59) and SICF with 32% reduction in mortality; top versus bottom SICF stratum 0.68, 0.53–0.88). Serum cotinine data revealed substantial recall bias of smoking history in persons with cognitive impairment. However analyses correcting for this bias did not alter the main conclusions: In a nationwide cohort of older Americans, analyses demonstrated a lower risk of death independent of confounders among those with high SICF scores and never smokers, without a significant interaction of the two

Development of Electrochemical Nanosensor for the Detection of Malaria Parasite in Clinical Samples

In this study, electrochemical nanosensors were developed from the synthesized metal oxide (MO) nanoparticles by supporting it on a gold electrode (Au). The activity of the developed nanosensor toward the detection of malaria biomarker (β-hematin) was determined and the optimum conditions at which the maximum detection and quantification occurred were established. β-Hematin current response at the sensors was higher when compared with the bare Au electrode and followed the order Au-CuO (C) &gt; Au-CuO (M) &gt; Au-Fe2O3 (M) &gt; Au-Fe2O3 (C) &gt; Au-Al2O3 (M) &gt; Au-Al2O3 (C) &gt; bare Au. The developed sensors were stable with a relatively low current drop (10.61–17.35 %) in the analyte. Au-CuO sensor had the best performance toward the biomarker and quantitatively detected P. berghei in infected mice's serum samples at 3.60–4.8 mM and P. falciparum in human blood serum samples at 0.65–1.35 mM concentration

Disclosing genetic risk for Alzheimer’s dementia to individuals with mild cognitive impairment

IntroductionThe safety of predicting conversion from mild cognitive impairment (MCI) to Alzheimer’s disease (AD) dementia using apolipoprotein E (APOE) genotyping is unknown.MethodsWe randomized 114 individuals with MCI to receive estimates of 3‐year risk of conversion to AD dementia informed by APOE genotyping (disclosure arm) or not (non‐disclosure arm) in a non‐inferiority clinical trial. Primary outcomes were anxiety and depression scores. Secondary outcomes included other psychological measures.ResultsUpper confidence limits for randomization arm differences were 2.3 on the State Trait Anxiety Index and 0.5 on the Geriatric Depression Scale, below non‐inferiority margins of 3.3 and 1.0. Moreover, mean scores were lower in the disclosure arm than non‐disclosure arm for test‐related positive impact (difference: ‐1.9, indicating more positive feelings) and AD concern (difference: ‐0.3).DiscussionProviding genetic information to individuals with MCI about imminent risk for AD does not increase risks of anxiety or depression and may provide psychological benefits.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154645/1/trc212002_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154645/2/trc212002.pd

Cognitive function, social integration and mortality in a U.S. national cohort study of older adults

<p>Abstract</p> <p>Background</p> <p>Prior research suggests an interaction between social networks and Alzheimer's disease pathology and cognitive function, all predictors of survival in the elderly. We test the hypotheses that both social integration and cognitive function are independently associated with subsequent mortality and there is an interaction between social integration and cognitive function as related to mortality in a national cohort of older persons.</p> <p>Methods</p> <p>Data were analyzed from a longitudinal follow-up study of 5,908 American men and women aged 60 years and over examined in 1988–1994 followed an average 8.5 yr. Measurements at baseline included self-reported social integration, socio-demographics, health, body mass index, C-reactive protein and a short index of cognitive function (SICF).</p> <p>Results</p> <p>Death during follow-up occurred in 2,431. In bivariate analyses indicators of greater social integration were associated with higher cognitive function. Among persons with SICF score of 17, 22% died compared to 54% of those with SICF score of 0–11 (p < 0.0001). After adjusting for confounding by baseline socio-demographics and health status, the hazards ratio (HR) (95% confidence limits) for low SICF score was 1.43 (1.13–1.80, p < 0.001). After controlling for health behaviors, blood pressure and body mass, C-reactive protein and social integration, the HR was 1.36 (1.06–1.76, p = 0.02). Further low compared to high social integration was also independently associated with increased risk of mortality: HR 1.24 (1.02–1.52, p = 0.02).</p> <p>Conclusion</p> <p>In a cohort of older Americans, analyses demonstrated a higher risk of death independent of confounders among those with low cognitive function and low social integration with no significant interaction between them.</p

A Randomized Controlled Trial of Disclosing Genetic Risk Information for Alzheimer’s Disease via Telephone

Purpose Telephone disclosure of genetic test results can improve access to services. To date, studies of its impact have focused on return of Mendelian risk information, principally hereditary cancer syndromes. Methods: In a multisite trial of Alzheimer’s disease genetic risk disclosure, asymptomatic adults were randomized to receive test results in-person or via telephone. Primary analyses examined patient outcomes 12 months after disclosure. Results: Data from 257 participants showed that telephone disclosure occurred 7.4 days sooner and were 30% shorter, on average, than in-person disclosure (both p<0.001). Anxiety and depression scores were well below cutoffs for clinical concern across protocols. Comparing telephone and in-person disclosure protocols, 99% CIs of mean differences were within non-inferiority margins on scales assessing anxiety, depression, and test-related distress, but inconclusive about positive impact. No differences were observed on measures of recall and subjective impact. Sub-analyses supported non-inferiority on all outcomes among APOE ε4-negative participants. Sub-analyses were inconclusive for APOE ε4-positive participants, although mean anxiety and depression scores were still well below cutoffs for clinical concern. Conclusion: Telephone disclosure of APOE results and risk for Alzheimer’s disease is generally safe and helps providers meet demands for services, even when results identify an increased risk for disease