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BackgroundOnline cognitive assessments are alternatives to in-clinic assessments.ObjectivesWe evaluated the relationship between online and in-clinic self-reported Everyday Cognition Scale (ECog).MethodsIn 94 Alzheimer's Disease Neuroimaging Initiative and Brain Health Registry (ADNI-BHR) participants, we estimated associations between online and in-clinic Everyday Cognition using Bland-Altman plots and regression. In 472 ADNI participants, we estimated reliability of in-clinic Everyday Cognition completed six months apart using Bland-Altman plots and regression.ResultsOnline Everyday Cognition associations: Mean difference was 0.11 (95% limits of agreement: -0.41 to 0.64). In-clinic Everyday Cognition score increased by 0.81 for each online Everyday Cognition score unit increase (R2=0.60). In-clinic Everyday Cognition reliability: Mean difference was 0.01 (95% limits of agreement: -0.61 to 0.62). In-clinic Everyday Cognition score at enrollment increased by 0.79 for each in-clinic Everyday Cognition score unit increase at six months (R2=0.61).ConclusionOnline Everyday Cognition closely corresponded with in-clinic Everyday Cognition, supporting validity of using online cognitive assessments to more efficiently facilitate Alzheimer's disease research.

BackgroundMidlife cardiovascular risk factors (CVRF) increase dementia risk. Less is known about whether CVRF identified before midlife impact late-life cognition in diverse populations.MethodsLinear regression models examined hypertension, hyperlipidemia, and overweight/obesity at ages 30 to 59 with late-life executive function, semantic memory, verbal episodic memory, and global cognition in a cohort of Asians, blacks, Latinos, and whites (n=1127; mean age=75.8, range=65 to 98). Models adjusted for age at CVRF, age at cognitive assessment, sex, race/ethnicity, participant education, and parental education.ResultsOverall, 34% had 1 CVRF at ages 30 to 59; 19% had 2+. Blacks (26%) and Latinos (23%) were more likely to have 2+ CVRF than Asians (14%) or whites (13%). Having 2+ CVRF was associated with lower global cognition [β=-0.33; 95% confidence interval (CI)=-0.45, -0.21], executive function (β=-0.26; 95% CI=-0.39, -0.13), verbal episodic memory (β=-0.34; 95% CI=-0.48, -0.20), and semantic memory (β=-0.20; 95% CI=-0.33, -0.07). Interaction by age (P=0.06) indicated overweight/obesity was negatively associated with executive function at ages 30 to 39 but not at ages 40 to 59. Race/ethnic-specific effects showed disparities in CVRF prevalence impact population disparities in late-life cognition.ConclusionBeing overweight/obese in early adulthood and having 2+ CVRF in early adulthood/midlife are modifiable targets to redress racial/ethnic disparities in cognitive impairment and dementia.

Post-traumatic stress disorder (PTSD) has been declared 'a life sentence' based on evidence that the disorder leads to a host of physical health problems. Some of the strongest empirical research - in terms of methodology and findings - has shown that PTSD predicts higher risk of cardiometabolic diseases, specifically cardiovascular disease (CVD) and type 2 diabetes (T2D). Despite mounting evidence, PTSD is not currently acknowledged as a risk factor by cardiovascular or endocrinological medicine. This view is unlikely to change absent compelling evidence that PTSD causally contributes to cardiometabolic disease. This review suggests that with developments in methods for epidemiological research and the rapidly expanding knowledge of the behavioral and biological effects of PTSD the field is poised to provide more definitive answers to questions of causality. First, we discuss methods to improve causal inference using the observational data most often used in studies of PTSD and health, with particular reference to issues of temporality and confounding. Second, we consider recent work linking PTSD with specific behaviors and biological processes, and evaluate whether these may plausibly serve as mechanisms by which PTSD leads to cardiometabolic disease. Third, we evaluate how looking more comprehensively into the PTSD phenotype provides insight into whether specific aspects of PTSD phenomenology are particularly relevant to cardiometabolic disease. Finally, we discuss new areas of research that are feasible and could enhance understanding of the PTSD-cardiometabolic relationship, such as testing whether treatment of PTSD can halt or even reverse the cardiometabolic risk factors causally related to CVD and T2D.

© 2015 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Int

© 2015 Macmillan Publishers Limited Objective:Higher late life body mass index (BMI) is unrelated to or even predicts lower risk of dementia in late life, a phenomenon that may be explained by reverse causation due to weight loss during preclinical phases

© 2015 The Authors.Clinical and population research on dementia and related neurologic conditions, including Alzheimer's disease, faces several unique methodological challenges. Progress to identify preventive and therapeutic strategies rests on valid and

Background: Despite moderate heritability estimates for depression-related phenotypes, few robust genetic predictors have been identified. Potential explanations for this discrepancy include the use of phenotypic measures taken from a single time point, ra

© 2014 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.Objective: To determine whether a polygenic risk score for Alzheimer's disease (AD) predicts dementia probability and memory functioning in non-Hispanic black (NHB) and non-Hispanic

Existing evidence on stress and asthma prevalence has disproportionately focused on pregnancy and postpregnancy early life stressors, largely ignoring the role of childhood adversity as a risk factor. Childhood adversity (neglect, stressful living conditio

Context: Anxiety disorders are common, with a lifetime prevalence of 20% in the U.S., and are responsible for substantial burdens of disability, missed work days and health care utilization. To date, no causal genetic variants have been identified for anxi