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Objectives:The present study examined differences in neurocognitive outcomes among non-Hispanic Black and White stroke survivors using the NIH Toolbox-Cognition Battery (NIHTB-CB), and investigated the roles of healthcare variables in explaining racial differences in neurocognitive outcomes post-stroke.Methods:One-hundred seventy adults (91 Black; 79 White), who participated in a multisite study were included (age:M=56.4;SD=12.6; education:M=13.7;SD=2.5; 50% male; years post-stroke: 1–18; stroke type: 72% ischemic, 28% hemorrhagic). Neurocognitive function was assessed with the NIHTB-CB, using demographically corrected norms. Participants completed measures of socio-demographic characteristics, health literacy, and healthcare use and access. Stroke severity was assessed with the Modified Rankin Scale.Results:An independent samplesttest indicated Blacks showed more neurocognitive impairment (NIHTB-CB Fluid Composite T-score:M=37.63;SD=11.67) than Whites (Fluid T-score:M=42.59,SD=11.54;p=.006). This difference remained significant after adjusting for reading level (NIHTB-CB Oral Reading), and when stratified by stroke severity. Blacks also scored lower on health literacy, reported differences in insurance type, and reported decreased confidence in the doctors treating them. Multivariable models adjusting for reading level and injury severity showed that health literacy and insurance type were statistically significant predictors of the Fluid cognitive composite (pp=.02, respectively) and significantly mediated racial differences on neurocognitive impairment.Conclusions:We replicated prior work showing that Blacks are at increased risk for poorer neurocognitive outcomes post-stroke than Whites. Health literacy and insurance type might be important modifiable factors influencing these differences. (JINS, 2017,23, 640–652)

Goal 1 of the National Plan to Address Alzheimer’s Disease is to prevent and effectively treat Alzheimer disease and Alzheimer disease–related dementias by 2025. To help inform the research agenda toward achieving this goal, the NIH hosts periodic summits that set and refine relevant research priorities for the subsequent 5 to 10 years. This proceedings article summarizes the 2016 Alzheimer's Disease–Related Dementias Summit, including discussion of scientific progress, challenges, and opportunities in major areas of dementia research, including mixed-etiology dementias, Lewy body dementia, frontotemporal degeneration, vascular contributions to cognitive impairment and dementia, dementia disparities, and dementia nomenclature.

Racial disparities in cognitive performance exist across the life course, but it is not known whether mediators of disparities differ by age. Understanding sources of cognitive disparities at different ages can inform policies and interventions. Data were obtained for non-Hispanic Black and White respondents to The National Survey of Midlife Development in the United States from 3 age groups: 28-44 (N = 1210; 20% Black); 45-64 (N = 2693; 15% Black); and 65-85 (N = 1298; 11% Black). Moderated mediation models characterized direct and indirect effects of race on episodic memory and executive function composite scores through economic, health, and psychosocial variables as a function of age group. Education, income, chronic health conditions, and external locus of control mediated cognitive disparities across the life course, although income was a stronger mediator at younger ages. Perceived discrimination was a weaker mediator among young adults due to an absence of racial differences in perceived discrimination in that group. Despite multiple indirect effects, there were still significant unexplained effects of race on cognition that were not moderated by age group. Interventional work is needed to determine whether increasing educational attainment and income, and reducing chronic health conditions and perceived constraints among Blacks, reduce cognitive disparities. Targeting income inequality and discrimination (or buffering the impact of those variables) may be differently effective at reducing cognitive disparities at different stages of the adult life course. (PsycINFO Database Record

Background We previously demonstrated that parietal lobe white matter hyperintensities (WMH) increase the risk for Alzheimer's disease (AD). Here, we examined whether individuals with apolipoprotein E gene ( APOE e4) have increased parietal WMH volume. Methods Participants were from the Washington Heights-Inwood Columbia Aging Project (WHICAP; n = 694, 47 with dementia) in northern Manhattan and the Etude Sante Psychologique Prevalence Risques et Traitement study (ESPRIT; n = 539, 8 with dementia) in Montpellier. The association between regional WMH and APOE e4 was examined separately in each group and then in a combined analysis. Results In WHICAP, e4 carriers had higher WMH volume particularly in parietal and occipital lobes. In ESPRIT, e4 carriers had elevated WMH particularly in parietal and temporal lobes. In the combined analysis, e4 carriers had higher WMH in parietal and occipital lobes. Increased WMH volume was associated with increased frequency of dementia irrespective of APOE e4 status; those with the e4 were more likely to have dementia if they also had increased parietal WMH. Conclusions APOE e4 is associated with increased parietal lobe WMH.

We examined whether the reserve capacity model can be extended to cognitive outcomes among older African Americans. Two hundred and ninety-two non-Hispanic Whites and 37 African Americans over age 54 participated in the normative study for the NIH Toolbox for the Assessment of Neurological and Behavioral Function. Multiple-group path analysis showed that associations between depressive symptoms and cognition differed by race, independent of age, education, reading level, income, health, and recruitment site. Depressive symptoms were associated with slowed processing speed among Whites and worse task-switching, inhibition, and episodic memory among African Americans. African Americans may be more vulnerable to negative effects of depression on cognition than non-Hispanic Whites. Further research is needed to explicate the psychological and neurobiological underpinnings of this greater vulnerability.

Microbleeds, small perivascular collections of hemosiderin manifested radiologically as hypointensities on gradient-echo magnetic resonance imaging (MRI), are important markers of small vessel pathology. Despite their clinical relevance, little is known about their prevalence and demographic correlates, particularly among ethnically diverse older adults. We examined demographic and clinical correlates of regional microbleeds in a multi-ethnic cohort and examined categorization schemes of microbleed distribution and severity.Between 2005 and 2007, 769 individuals participated in a MRI study as part of the Washington Heights/Inwood Columbia Aging Project. Approximately four years later, 243 out of 339 participants (mean age=84.50) who returned for a repeat MRI had gradient-echo scans for microbleed assessment and comprised the sample. We examined the association of deep and lobar microbleeds with age, sex, education, vascular factors, cognitive status and markers of small vessel disease.Sixty-seven of the 243 (27%) participants had at least one microbleed. Individuals with microbleeds were more likely to have a history of stroke than individuals without. When categorized as having either no microbleeds, microbleeds in deep regions only, in lobar regions only, and both deep and lobar microbleeds, hypertension, proportion of strokes, and white matter hyperintensity volume (WMH) increased monotonically across the four groups. The number of lobar microbleeds correlated with WMH volume and diastolic blood pressure.Microbleeds in deep and lobar locations are associated with worse outcomes than microbleeds in either location alone, although the presence of lobar microbleeds appears to be more clinically relevant.

Objective The present study aimed to investigate whether cognitive reserve moderated the association between depressive symptoms and cognition, as well as brain volumes in a sample of older adults. Methods Non-demented participants (n = 3484) were selected from the Washington Heights/Hamilton Heights Inwood Columbia Aging Project (Northern Manhattan). A subsample of these participants without dementia (n = 703), who had brain imaging data, was also selected for a separate analysis. Depressive symptomatology was assessed with the 10-item Center for Epidemiologic Studies Depression Scale. Reading level and years of education were used as measures of cognitive reserve. Four distinct cognitive composite scores were calculated: executive function, memory, visual–spatial, and language. Results Multiple regression analysis revealed interaction effects between both measures of cognitive reserve and depressive symptoms on all the cognitive outcome measures except for visual–spatial ability. Those with greater reserve showed greater cognitive decrements than those with lower levels of reserve as depressive symptoms increased. A borderline interaction effect was revealed between reading level and depressive symptoms on total brain volumes. Those with lower reading scores showed greater volume loss as depressive symptoms increased than those with higher reading scores. Conclusions Our findings indicate that the association between late-life depressive symptoms and core aspects of cognition varies depending on one's level of cognitive reserve. Those that had greater levels of education and/or reading ability showed a greater decrease in memory, executive, and language performances as depressive symptoms increased than those with lower years of education and reading ability. Copyright © 2014 John Wiley & Sons, Ltd.

The National Alzheimer's Project Act, signed into law in 2011, mandates a National Plan to Address Alzheimer's Disease that is updated annually. In the Plan, the term Alzheimer disease includes not only Alzheimer disease (AD) proper, but also several specified related dementias, namely, frontotemporal, Lewy body, vascular, and mixed dementia. In response to a specific action item in the 2012 National Plan, the National Institute of Neurological Disorders and Stroke, in collaboration with the National Institute on Aging, convened panels of experts and conducted a 2-day public conference to develop research priorities and timelines for addressing Alzheimer disease–related dementias (ADRD) in 5 topic areas: multiple etiology dementias, health disparities, Lewy body dementias including dementia with Lewy bodies and Parkinson disease dementia, frontotemporal dementia and related tauopathies, and vascular contributions to ADRD. By design, the product was up to 8 prioritized research recommendations in each topic area including estimated timelines from when work on a recommendation is started to completion or to full implementation of an ongoing activity, and recognition of shared research themes across recommendations. These included increased education and training of both researchers and health care professionals, addressing health disparities, fundamental neurobiology research, advanced diagnostics, collaborative biosample repositories, and a focus on developing effective interventions to prevent or treat ADRD by the year 2025 as targeted by the National Plan.

Racial disparities in late-life cognitive test performance are well documented (Alley, Suthers, & Crimmins, 2007; Fillenbaum et al., 2001; Masel & Peek, 2009; Masel, Raji, & Peek, 2010; Rodgers, Ofstedal, & Herzog, 2003; Schwartz et al., 2004; Zsembik & Peek, 2001). Studies have shown that nondemented black older adults demonstrate lower cognitive test performance compared with white peers. These disparities are sometimes attenuated by demographic factors such as educational attainment and socioeconomic status (Barnes et al., 2011; Schwartz et al., 2004) or other predictors of cognitive function such as physical activity (Masel et al., 2010), occupational attainment (Manly et al., 1998), occupational prestige (Albert, 1995; Del Ser, Hachinsky, Merskey, & Munoz, 1999; Fratiglioni, 1996; Friedland, 1993; Katzman, 1993), and health-related variables (Manly et al., 1998; Mungas et al., 2009). Some studies suggest that race-related differences in late-life cognitive performance are sometimes (Fillenbaum et al., 2001), but not typically, eliminated by accounting for such variables. Literacy in late life, though highly correlated with years of education (Verhaeghen, 2003), has proven to be a stronger predictor of late-life cognitive functioning than years of education, especially for blacks (Dotson, Kitner-Triolo, Evans, & Zonderman, 2009). Adjusting for literacy has also been shown to greatly attenuate the estimated effect of race and to eliminate most racial differences on neuropsychological test performance in multiethnic elderly samples matched on years of education (Manly et al., 1999; Manly, Jacobs, Touradji, Small, & Stern, 2002; Touradji, Manly, Jacobs, & Stern, 2001). Literacy has been proposed to be a better predictor of late-life cognitive differences than years of education, especially for minorities, because it better approximates the cognitive benefits conferred by the early-life educational experience. Educational experiences can be characterized with respect to duration, for example, using years of schooling completed or degrees attained, or with respect to quality of schooling. The degree of cognitive benefit from education may better correspond with indices of educational quality than measures of educational attainment (Dotson et al., 2009). As Manly, Touradji, Tang, and Stern (2003) demonstrated, educational quality as approximated by literacy in later life is a stronger predictor of late-life cognitive performance than years of education. Evidence also suggests that educational quality, measured by state education policies, independently predicts late-life differences in cognition (Glymour, 2004). Historically, educational quality has varied widely across states and over time in the United States (Berkman & Glymour, 2006), with pronounced differences especially between northern and southern parts of the country. A majority of adults now aged 50 and older grew up during the influence of Jim Crow laws. Many blacks received their education in the South, where social conditions differed greatly from the North (Barnes, 1983). For example, most Southerners attended segregated schools, and schools for black students offered significantly lower quality education than schools for whites (Glymour & Manly, 2008). Because many of today’s black elders attended school under Jim Crow laws in segregated schools, race-based differences in educational quality may account for a substantial portion of the racial differences observed in late-life cognition. It is difficult to collect direct data on the quality of education received many decades ago, but recent research has taken advantage of historical state and local laws and records. For example, Lleras-Muney (2002) found that state-level compulsory school attendance laws predicted mortality in addition to average years of education completed for people born in a state. Related to the present study, Glymour (2004) found that individuals born in states that had high levels of mandatory schooling performed better on cognitive testing decades after finishing school, after controlling for demographic characteristics. This finding suggests that historical indices of early-life educational experiences, albeit imprecise on an individual level, may partly explain cognitive performance in later life. Considering the significant social and educational disparities that existed during early childhood for today’s older adults, state laws dictating educational policy, as well as other indices of educational quality (e.g., classroom size, student:teacher ratio), may independently explain a substantial portion of race-based differences in late-life cognition. The WHICAP (Washington Heights-Inwood Columbia Aging Project) study, used in the present study, is a community-based study of cognitive aging in a multiethnic population of communities in New York City. WHICAP measured several individual- and state-level characteristics of early-life educational quality and collected individual-level measures of cognition and literacy during late life. The present study examined the utility of both early-life educational quality and literacy in explaining race-related differences in late-life cognitive performance within the WHICAP sample. We hypothesized that both educational quality and literacy account for a significant amount of the variance in general and domain-specific late-life cognitive performance, and both factors significantly attenuate the apparent racial disparities in level and pace of change in late-life cognitive functioning. We hypothesized that literacy is a stronger predictor of late-life cognitive functioning than educational quality for two reasons. First, literacy was measured more proximally to cognitive outcomes. Second, many indicators of early-life educational quality were obtained based on state records at the time participants were in school, and such area-level measures typically show weaker associations than those obtained at the individual level.

Socioeconomic disadvantages in childhood has been linked to dementia in late life. However, the underlying pathways through which childhood socioeconomic status (CSES) affects health in old age is unclear. CSES has been linked to age-related differences in regions affected by Alzheimer’s disease (AD; e.g., hippocampus). CSES varies across race/ethnicity; It is critical to examine the relationship between CSES and age-related brain structural changes across diverse aging populations. We used an established proxy for CSES, number of siblings (i.e., sibship size), to examine whether CSES buffered age-related changes in hippocampal volume in a community-based sample of racially/ethnically diverse older adults. Sibship size moderated age-related differences in hippocampal volume in Whites (β=-5.61[-11.09,-0.12]), but not in Blacks and Hispanics. Results indicate that Whites with no sibling (vs. Whites with siblings) show less age-related difference in hippocampal volume. Future analyses will examine other CSES factors (i.e., parental education/occupation) on age-related structural changes across race/ethnicity.

Objective The NIH Toolbox for Assessment of Neurological and Behavioral Function (NIHTB) was developed under contract from the National Institutes of Health to create a set of easy-to-administer neuropsychological measures, for use across the lifespan (ages 3-85). The NIHTB Cognition Battery (NIHTB-CB) includes two language measures that were developed, calibrated, and normed separately in English and Spanish. This analysis presents the test-retest reliability and construct validity of the Spanish-language picture vocabulary test (S-PVT) and oral reading recognition test (S-ORRT) among adults. Participants and Method Participants were adults age 18-85 who took part in the NIHTB norming study in Spanish (N = 408, Age: M = 44.1, SD = 16.7; Education: M = 10.7, SD = 4.3; 65.0% female). Of these, 48 repeated the battery 1 week later. Both the S-PVT and the S-ORRT were administered using computer adaptive testing and scored using item response theory. Spearman’s correlations were used to evaluate test-retest reliability. Convergent validity was evaluated by correlating S-PVT scores with scores on the Batería-III Woodcock-Muñoz Vocabulario Sobre Dibujos, and by correlating S-ORRT scores with scores on a 48-item version of the Word Accentuation Test. Adjusted Spearman’s correlations and general linear models related scores to age, education, and sex. Results Both the S-PVT (ρ = 0.87, p < .001) and the S-ORRT (ρ = 0.88, p < .001) demonstrated good test-retest reliability. Good convergent validity was found for both the S-PVT (ρ = 0.76, p < .001) and the S-ORRT (ρ = 0.65, p < .001). Scores on the S-PVT were positively related to education (ρ = 0.38, p < .001), and scores on the S-ORRT were negatively related to age (ρ = -0.18, p < .01) and positively related to education (ρ = 0.30, p < .001). Conclusions The Spanish language measures of the NIHTB-CB demonstrated acceptable reliability and validity, suggesting they can be used to measure language ability among Spanish-speaking adults in the United States.

Objective Bilinguals may be able to retain similar levels of cognitive functioning given age and/or Alzheimer’s Disease-related neurodegeneration, compared to monolinguals. Many studies have yielded equivocal findings that may be explained by within-group differences among bilinguals, such as frequency of language use. The current study aimed to clarify the role of frequency of bilingual language use (i.e., active versus passive) in the association of brain structure and memory. We hypothesized that active bilinguals would demonstrate better memory performance compared to passive bilinguals and monolinguals, and that active bilingualism would buffer the effects of temporal lobe integrity on memory. Participants and Method In a longitudinal aging study, 217 older Hispanic adults (Age M = 74 years, SD = 6; 70% women) underwent neuropsychological evaluation and 1.5T MR imaging. Bilingualism was determined by self-reported use of English and Spanish. Active bilinguals reported using both languages daily. Multiple regression tested main effects and interactions of bilingualism and entorhinal cortical thickness on semantic and episodic memory, adjusted for age, sex/gender, and education. Results Bilingualism was associated with better semantic memory(F[2,209] = 6.25, p = .002) but not with episodic memory(F[2,209)] = 0.34, p = .71). There was a significant bilingualism X entorhinal cortical thickness interaction on semantic memory (β = -.26, p = .02), indicating that active bilinguals were better able to maintain cognitive functioning with lower cortical thickness, compared to passive bilinguals and monolinguals. Conclusions Active bilingualism may protect semantic memory against cortical thinning of the entorhinal cortex. Future studies will explore whether this relationship remains after accounting for additional environmental and sociocultural factors (e.g., immigrant status) that influence the ability or opportunity to become bilingual, and whether active bilingualism affects cognitive trajectory in late life.

Objective The “healthy immigrant effect” pertains to findings that Hispanics/Latinos born outside of the US tend to be physically and emotionally healthier than individuals born in the US. However, immigrant Latino groups residing in the US have higher incidences of dementia (Tang et al., 2001). Sex/gender and years of education have been found to moderate the relationship between age of migration and cognitive functioning among immigrants born in Mexico (Garcia et al., 2017; Hill et al., 2012). While years of education has been the focus of many studies, literacy (ability to read/write) has been less frequently explored as a moderator of age of migration and cognitive change. We investigated the effect of age of migration on cognitive trajectory in a diverse Latino population and explored whether literacy influences the association between age of immigration and cognitive change. We hypothesize that literacy (ability to read/write) will buffer the effects of age of migration on cognitive (memory, language, motor speed, visuospatial) trajectory. Participants and Method Age at baseline, English fluency, country of birth, sex/gender, and years of education were included as time-invariant covariates and literacy was tested as a moderator via multiple group modeling. Results Results show that age of migration is marginally and inversely associated with baseline cognitive performance (p < .01). Thus, individuals who immigrated at an older age had lower baseline cognitive scores than their counterparts. Age of migration was not associated with cognitive change. Independent of covariates, literacy did not buffer the negative effects of later age at migration on cognitive function. Conclusions Results suggest that literacy confers a small advantage in premorbid cognition, but does not protect against cognitive decline over time. These findings also suggest that adults who immigrate at an older age present with lower cognitive scores at baseline, but do not experience faster rates of cognitive change. References Tang, M. X., Cross, P., Andrews, H., Jacobs, D. M., Small, S., Bell, K., ... & Mayeux, R. (2001). Incidence of AD in African-Americans, Caribbean Hispanics, and Caucasians in northern Manhattan. Neurology, 56, 49-56. Garcia, M. A., Reyes, A. M., Downer, B., Saenz, J. L., Samper-Ternent, R. A., & Raji, M. (2018). Age of migration and the incidence of cognitive impairment: A cohort study of elder Mexican-Americans. Innovation in aging, 1, igx037. https://doi.org/10.1093/geroni/igx037. Hill, T. D., Angel, J. L., Balistreri, K. S., & Herrera, A. P. (2012). Immigrant Status and Cognitive Functioning in Late Life: An Examination of Gender Variations in the Healthy Immigrant Effect. Social Science & Medicine (1982), 75, 2076–2084. http://doi.org/10.1016/j.socscimed.2012.04.005.

IMPORTANCE: Genetic causes of late-onset Alzheimer disease (LOAD) are not completely explained by known genetic loci. Whole-exome and whole-genome sequencing can improve the understanding of the causes of LOAD and provide initial steps required to identify potential therapeutic targets. OBJECTIVE: To identify the genetic loci for LOAD across different ethnic groups. DESIGN, SETTING, AND PARTICIPANTS: This multicenter cohort study was designed to analyze whole-exome sequencing data from a multiethnic cohort using a transethnic gene-kernel association test meta-analysis, adjusted for sex, age, and principal components, to identify genetic variants associated with LOAD. A meta-analysis was conducted on the results of 2 independent studies of whole-exome and whole-genome sequence data from individuals of European ancestry. This group of European American, African American, and Caribbean Hispanic individuals participating in an urban population-based study were the discovery cohort; the additional cohorts included affected individuals and control participants from 2 publicly available data sets. Replication was achieved using independent data sets from Caribbean Hispanic families with multiple family members affected by LOAD and the International Genetics of Alzheimer Project. MAIN OUTCOMES AND MEASURES: Late-onset Alzheimer disease. RESULTS: The discovery cohort included 3595 affected individuals, while the additional cohorts included 5931 individuals with LOAD and 5504 control participants. Of 3916 individuals in the discovery cohort, we included 3595 individuals (1397 with LOAD and 2198 cognitively healthy controls; 2451 [68.2%] women; mean [SD] age, 80.3 [6.83] years). Another 321 individuals (8.2%) were excluded because of non-LOAD diagnosis, age younger than 60 years, missing covariates, duplicate data, or genetic outlier status. Gene-based tests that compared affected individuals (n = 7328) and control participants (n = 7702) and included only rare and uncommon variants annotated as having moderate-high functional effect supported PINX1 (8p23.1) as a locus with gene-wide significance (P = 2.81 × 10(−6)) after meta-analysis across the 3 studies. The PINX1 finding was replicated using data from the family-based study and the International Genetics of Alzheimer Project. Full meta-analysis of discovery and replication cohorts reached a P value of 6.16 × 10(−7) for PINX1 (in 7620 affected individuals vs 7768 control participants). We also identified TREM2 in an annotation model that prioritized highly deleterious variants with a combined annotation dependent depletion greater than 20 (P= 1.0 × 10(−7)). CONCLUSIONS AND RELEVANCE: This gene-based, transethnic approach identified PINX1, a gene involved in telomere integrity, and TREM2, a gene with a product of an immune receptor found in microglia, as associated with LOAD. Both genes have well-established roles in aging and neurodegeneration.

This monograph presents the pediatric portion of the National Institutes of Health (NIH) Toolbox Cognition Battery (CB) of the NIH Toolbox for the Assessment of Neurological and Behavioral Function. The NIH Toolbox is an initiative of the Neuroscience Blueprint, a collaborative framework through which 16 NIH Institutes, Centers, and Offices jointly support neuroscience-related research, to accelerate discoveries and reduce the burden of nervous system disorders. The CB is one of four modules that measure cognitive, emotional, sensory, and motor health across the lifespan. The CB is unique in its continuity across childhood, adolescence, early adulthood, and old age, and in order to help create a common currency among disparate studies, it is also available at low cost to researchers for use in large-scale longitudinal and epidemiologic studies. This chapter describes the evolution of the CB; methods for selecting cognitive subdomains and instruments; the rationale for test design; and a validation study in children and adolescents, ages 3-15 years. Subsequent chapters feature detailed discussions of each test measure and its psychometric properties (Chapters 2-6), the factor structure of the test battery (Chapter 7), the effects of age and education on composite test scores (Chapter 8), and a final summary and discussion (Chapter 9). As the chapters in this monograph demonstrate, the CB has excellent psychometric properties, and the validation study provided evidence for the increasing differentiation of cognitive abilities with age.

The theory of cognitive reserve attempts to explain why some individuals are more resilient to age-related brain pathology. Efforts to explore reserve have been hindered by measurement difficulties. Reed et al. (2010) proposed quantifying reserve as residual variance in episodic memory performance that remains after accounting for demographic factors and brain pathology (whole brain, hippocampal, and white matter hyperintensity volumes). This residual variance represents the discrepancy between an individual's predicted and actual memory performance. The goals of the present study were to extend these methods to a larger, community-based sample and to investigate whether the residual reserve variable is explained by age, predicts longitudinal changes in language, and predicts dementia conversion independent of age. Results support this operational measure of reserve. The residual reserve variable was associated with higher reading ability, lower likelihood of meeting criteria for mild cognitive impairment, lower odds of dementia conversion independent of age, and less decline in language abilities over 3 years. Finally, the residual reserve variable moderated the negative impact of memory variance explained by brain pathology on language decline. This method has the potential to facilitate research on the mechanisms of cognitive reserve and the efficacy of interventions designed to impart reserve. (JINS, 2013, 19, 1–9)

Motor function involves complex physiologic processes and requires the integration of multiple systems, including neuromuscular, musculoskeletal, and cardiopulmonary, and neural motor and sensory-perceptual systems. Motor-functional status is indicative of current physical health status, burden of disease, and long-term health outcomes, and is integrally related to daily functioning and quality of life. Given its importance to overall neurologic health and function, motor function was identified as a key domain for inclusion in the NIH Toolbox for Assessment of Neurological and Behavioral Function (NIH Toolbox). We engaged in a 3-stage developmental process to: 1) identify key subdomains and candidate measures for inclusion in the NIH Toolbox, 2) pretest candidate measures for feasibility across the age span of people aged 3 to 85 years, and 3) validate candidate measures against criterion measures in a sample of healthy individuals aged 3 to 85 years (n = 340). Based on extensive literature review and input from content experts, the 5 subdomains of dexterity, strength, balance, locomotion, and endurance were recommended for inclusion in the NIH Toolbox motor battery. Based on our validation testing, valid and reliable measures that are simultaneously low-cost and portable have been recommended to assess each subdomain, including the 9-hole peg board for dexterity, grip dynamometry for upper-extremity strength, standing balance test, 4-m walk test for gait speed, and a 2-minute walk test for endurance.

Objective: To evaluate the association of late-life depression with mild cognitive impairment (MCI) and dementia in a multiethnic community cohort. Design and Setting: A cohort study was conducted in Northern Manhattan, New York, New York. Participants: A total of 2160 community-dwelling Medicare recipients aged 65 years or older were included in the study. Methods: Depression was assessed using the 10-item version of the Center for Epidemiological Studies Depression scale (CES-D) and defined by a CES-D score of 4 or more. We used logistic regression for cross-sectional association analyses and proportional hazards regression for longitudinal analyses. Main Outcome Measures: Mild cognitive impairment dementia, and progression from MCI to dementia were the main outcome measures. We also used subcategories of MCI (amnestic and nonamnestic), and dementia (probable Alzheimer disease and vascular dementia, including possible Alzheimer disease with stroke). Results: Baseline depression was associated with prevalent MCI (odds ratio, 1.4; 95% CI, 1.1-1.9) and dementia (2.2; 1.6-3.1). Baseline depression was associated with an increased risk of incident dementia (hazard ratio [HR], 1.7; 95% CI, 1.2-2.3) but not with incident MCI (0.9; 0.7-1.2). Persons with MCI and coexisting depression at baseline had a higher risk of progression to dementia (HR, 2.0; 95% CI, 1.2-3.4), especially vascular dementia (4.3; 1.1-17.0), but not Alzheimer disease (1.9; 1.0-3.6). Conclusion: The association of depression with prevalent MCI and with progression from MCI to dementia, but not with incident MCI, suggests that depression accompanies cognitive impairment but does not precede it. JAMA Neurol. 2013;70(3):383-389. Published online December 31, 2012. doi:10.1001/jamaneurol.2013.603

OBJECTIVE We examined the association of the Diabetes Prevention Program (DPP) intervention arms (lifestyle intervention, metformin, and placebo) with cognition in the Diabetes Prevention Program Outcomes Study (DPPOS). We also examined metformin use, incident type 2 diabetes, and glycemia as exposures. RESEARCH DESIGN AND METHODS The DPP lasted 2.8 years, followed by a 13-month bridge to DPPOS. Cognition was assessed in DPPOS years 8 and 10 (12 and 14 years after randomization) with the Spanish English Verbal Learning Test (SEVLT), letter fluency and animal fluency tests, Digit Symbol Substitution Test (DSST), and a composite cognitive score. RESULTS A total of 2,280 participants (749 lifestyle, 776 metformin, and 755 placebo) aged 63.1 ± 10.7 years underwent cognitive assessments; 67.7% women, 54.6% non-Hispanic white, 20.7% non-Hispanic black, 14.6% Hispanic, 5.5% American Indian, and 4.6% Asian; 26.6% were homozygous or heterozygous for APOE-ε4. At the time of cognitive assessment, type 2 diabetes was higher in the placebo group (57.9%; P < 0.001) compared with lifestyle (47.0%) and metformin (50.4%). Metformin exposure was higher in the metformin group (8.72 years; P < 0.001) compared with placebo (1.43 years) and lifestyle (0.96 years). There were no differences in cognition across intervention arms. Type 2 diabetes was not related to cognition, but higher glycated hemoglobin at year 8 was related to worse cognition after confounder adjustment. Cumulative metformin exposure was not related to cognition. CONCLUSIONS Exposure to intensive lifestyle intervention or metformin was not related to cognition among DPPOS participants. Higher glycemia was related to worse cognitive performance. Metformin seemed cognitively safe among DPPOS participants.

Introduction African Americans' (AAs) late-onset Alzheimer's disease (LOAD) genetic risk profile is incompletely understood. Including clinical covariates in genetic analyses using informed conditioning might improve study power. Methods We conducted a genome-wide association study (GWAS) in AAs employing informed conditioning in 1825 LOAD cases and 3784 cognitively normal controls. We derived a posterior liability conditioned on age, sex, diabetes status, current smoking status, educational attainment, and affection status, with parameters informed by external prevalence information. We assessed association between the posterior liability and a genome-wide set of single-nucleotide polymorphisms (SNPs), controlling for APOE and ABCA7 , identified previously in a LOAD GWAS of AAs. Results Two SNPs at novel loci, rs112404845 ( P = 3.8 × 10 −8 ), upstream of COBL , and rs16961023 ( P = 4.6 × 10 −8 ), downstream of SLC10A2 , obtained genome-wide significant evidence of association with the posterior liability. Discussion An informed conditioning approach can detect LOAD genetic associations in AAs not identified by traditional GWAS.

Objective:To investigate the association between a genetic risk score (GRS) and familial late-onset Alzheimer disease (LOAD) and its predictive value in families multiply affected by the disease.Methods:Using data from the National Institute on Aging Genetics Initiative for Late-Onset Alzheimer Disease (National Institute on Aging–Late-Onset Alzheimer's Disease Family Study), mixed regression models tested the association of familial LOAD with a GRS based on single nucleotide polymorphisms (SNPs) previously associated with LOAD. We modeled associations using unweighted and weighted scores with estimates derived from the literature. In secondary models, we adjusted subsequent models for presence of the APOE ε4 allele and further tested the interaction between APOE ε4 and the GRS. We constructed a similar GRS in a cohort of Caribbean Hispanic families multiply affected by LOAD by selecting the SNP with the strongest p value within the same regions.Results:In the NIA-LOAD families, the GRS was significantly associated with LOAD (odds ratio [OR] 1.29; 95% confidence interval 1.21–1.37). The results did not change after adjusting for APOE ε4. In Caribbean Hispanic families, the GRS also significantly predicted LOAD (OR 1.73; 1.57–1.93). Higher scores were associated with lower age at onset in both cohorts.Conclusions:High GRS increases the risk of familial LOAD and lowers the age at onset, regardless of ethnic group.

Background: Previous research has identified multiple risk and protective factors for late onset Alzheimer’s disease (LOAD). However, it is not known whether these risk and protective factors differ for individuals who are cognitively stable versus those already experiencing declines. Objective: This study examined how dementia risk factors differ across subgroups of older adults defined by memory trajectory. This line of research may lead to more individualized risk profiles. Methods: Risk factors for incident LOAD were compared across previously-validated groups of older adults exhibiting different memory trajectories (“Stable-High,” “Stable-Low,” “Decliner,” “Rapid Decliner”) using stratified Cox regressions. Participants included 2,593 racially/ethnically diverse older adults (mean age of 76 at study entry) in the Washington HeightsInwood Columbia Aging Project. Results: Predictors of incident dementia differed across trajectory groups: older age only incurred independent risk in stable groups, education did not incur independent protection in the rapidly declining group, depression only incurred independent risk in the stable-low group, stroke incurred independent risk in the two extreme groups, and APOE-4 only incurred independent risk in the rapidly declining group. Conclusion: The finding that different risk factors for LOAD were associated with specific memory trajectories may reflect the existence of resilience or vulnerability factors that modify the individual influences of risk/protective factors. This study highlights the utility of considering interactions between dementia risk factors and a patient’s unique cognitive history.

OBJECTIVE This study aimed to examine the association between self-reported sleep problems and cognitive decline in community-dwelling older people. We hypothesized that daytime somnolence predicts subsequent cognitive decline. METHODS This is a longitudinal study in a 3.2-year follow-up, with 18-month intervals. The setting is the Washington Heights-Inwood Community Aging Project. There were 1098 participants, who were over 65 years old and recruited from the community. Sleep problems were estimated using five sleep categories derived from the RAND Medical Outcome Study Sleep Scale: sleep disturbance, snoring, awaken short of breath/with a headache, sleep adequacy, and daytime somnolence. Four distinct cognitive composite scores were calculated: memory, language, speed of processing, and executive functioning. We used generalized estimating equations analyses with cognitive scores as the outcome, and time, sleep categories and their interactions as the main predictors. Models were initially unadjusted and then adjusted for age, gender, education, ethnicity, depression, and apolipoprotein E-e4 genotype. RESULTS Increased daytime somnolence (including feeling drowsy/sleepy, having trouble staying awake, and taking naps during the day) was linked to slower speed of processing both cross-sectionally (B = -0.143, p = 0.047) and longitudinally (B = -0.003, p = 0.027). After excluding the demented participants at baseline, the results remained significant (B = -0.003, p = 0.021). CONCLUSIONS Our findings suggest that daytime somnolence may be an early sign of cognitive decline in the older population.

The Alzheimer’s Disease Neuroimaging Initiative (ADNI) is a large multi-center study designed to develop optimized methods for acquiring longitudinal neuroimaging, cognitive, and biomarker measures of AD progression in a large cohort of patients with Alzheimer’s disease (AD), patients with mild cognitive impairment, and healthy controls. Detailed neuropsychological testing was conducted on all participants. We examined the factor structure of the ADNI Neuropsychological Battery across older adults with differing levels of clinical AD severity based on the Clinical Dementia Rating Scale (CDR). Confirmatory factor analysis (CFA) of 23 variables from 10 neuropsychological tests resulted in five factors (memory, language, visuospatial functioning, attention, and executive function/processing speed) that were invariant across levels of cognitive impairment. Thus, these five factors can be used as valid indicators of cognitive function in older adults who are participants in ADNI.

The goal of the current study was to examine cognitive change in both healthy controls (n = 229) and individuals with mild cognitive impairment (MCI) (n = 397) from the Alzheimer's Disease Neuroimaging Initiative (ADNI). We applied latent growth modeling to examine baseline and longitudinal change over 36 months in five cognitive factors derived from the ADNI neuropsychological test battery (memory, executive function/processing speed, language, attention and visuospatial). At baseline, MCI patients demonstrated lower performance on all of the five cognitive factors when compared to controls. Both controls and MCI patients declined on memory over 36 months; however, the MCI patients declined at a significantly faster rate than controls. The MCI patients also declined over 36 months on the remaining four cognitive factors. In contrast, the controls did not exhibit significant change over 36 months on the non-memory cognitive factors. Within the MCI group, executive function declined faster than memory, while the other factor scores changed slower than memory over time. These findings suggest different patterns of cognitive change in healthy older adults and MCI patients. The findings also suggest that, when compared with memory, executive function declines faster than other cognitive factors in patients with MCI. Thus, decline in non-memory domains may be an important feature for distinguishing healthy older adults and persons with MCI.

Hepatitis C (HCV) is the most common cause of chronic liver damage in the United States [1]. Many patients are infected with both HCV and HIV; rates of co-infection range from 16–40% with higher rates in intravenous drug abusers [2–3]. In the last decade, several studies have suggested that patients with HCV have a high prevalence of cognitive impairments, and that the effects on cognition are unrelated to hepatic encephalopathy [see reviews within 3,4]. Autopsy studies have shown replicative forms of HCV virus in the brain of some HCV patients [5–7], and brain magnetic resonance spectroscopy studies demonstrated patterns consistent with inflammation in the basal ganglia and white matter [8–9]. Moreover, several studies have suggested that co-infection with HCV and HIV may have worse effects on cognition than monoinfection [10,11]. Nonetheless, most previous series of the effects of HCV and HIV on cognition have been small; often too small to control for the numerous confounding factors that influence cognition. At least 2 larger studies that attempted to control for these confounding factors, did not find a significant effect for HCV infection [2,12]. Women were underrepresented in most previous studies of the effects of HCV and HIV on cognition, and some have suggested that HIV-related cognitive impairment is worse in women [13]. Because HCV is prevalent in the large women’s interagency HIV study (WIHS), we assessed the effects of HCV and HIV on cognition in analyses.

We examined the influence of neighborhood socioeconomic position (SEP), racial/ethnic composition, and living in a major city on cognitive trajectories and intervention outcomes. Data came from the Advanced Cognitive Training for Independent and Vital Elderly study ( N = 2,438). Mixed effects analyses examined the associations between neighborhood variables and memory, reasoning, speed of processing, and everyday cognition, estimating differences in initial gains (potentially related to practice) and long-term rate of change over 10 years. The effect of reasoning training on initial gain was weaker for individuals in a major city. For everyday cognition, there was a stronger initial gain for memory-trained and control participants in areas with more racial/ethnic minorities and for speed-trained and control individuals in higher SEP areas. The racial/ethnic minority effect was no longer significant after adjustment for multiple comparisons. Neighborhood factors may be more important in practice-related improvement than in long-term change.

The objective of the study was to examine variability across multiple prospective cohort studies in level and rate of cognitive decline by race/ethnicity and years of education. We compare data across studies, we harmonized estimates of common latent factors representing overall or general cognitive performance, memory, and executive function derived from the: (a) Washington Heights, Hamilton Heights, Inwood Columbia Aging Project (N = 4,115), (b) Spanish and English Neuropsychological Assessment Scales (N = 525), (c) Duke Memory, Health, and Aging study (N = 578), and (d) Neurocognitive Outcomes of Depression in the Elderly (N = 585). We modeled cognitive change over age for cognitive outcomes by race, education, and study. We adjusted models for sex, dementia status, and study-specific characteristics. The results found that for baseline levels of overall cognitive performance, memory, and executive function, differences in race and education tended to be larger than between-study differences and consistent across studies. This pattern did not hold for rate of cognitive decline: effects of education and race/ethnicity on cognitive change were not consistently observed across studies, and when present were small, with racial/ethnic minorities and those with lower education declining at faster rates. In this diverse set of datasets, non-Hispanic Whites and those with higher education had substantially higher baseline cognitive test scores. However, differences in the rate of cognitive decline by race/ethnicity and education did not follow this pattern. This study suggests that baseline test scores and longitudinal change have different determinants, and future studies to examine similarities and differences of causes of cognitive decline in racially/ethnically and educationally diverse older groups is needed.

Although the relationship between education and cognitive status is well-known, evidence regarding whether education moderates the trajectory of cognitive change in late life is conflicting. Early studies suggested that higher levels of education attenuate cognitive decline. More recent studies using improved longitudinal methods have not found that education moderates decline. Fewer studies have explored whether education exerts different effects on longitudinal changes within different cognitive domains. In the present study, we analyzed data from 1014 participants in the Victoria Longitudinal Study to examine the effects of education on composite scores reflecting verbal processing speed, working memory, verbal fluency, and verbal episodic memory. Using linear growth models adjusted for age at enrollment (range, 54–95 years) and gender, we found that years of education (range, 6–20 years) was strongly related to cognitive level in all domains, particularly verbal fluency. However, education was not related to rates of change over time for any cognitive domain. Results were similar in individuals older or younger than 70 at baseline, and when education was dichotomized to reflect high or low attainment. In this large longitudinal cohort, education was related to cognitive performance but unrelated to cognitive decline, supporting the hypothesis of passive cognitive reserve with aging. (JINS, 2011, 17, 1039–1046)

OBJECTIVES: To cross-sectionally quantify the contribution of proxy measures of cognitive reserve reflective of the lifespan, such as education, socioeconomic status (SES), reading ability, and cognitive activities, in explaining late-life cognition. DESIGN: Prospective observational cohort study of aging. SETTING: Retirement communities across the Chicago metropolitan area. PARTICIPANTS: Nine hundred fifty-one older adults free of clinical dementia in the Rush Memory and Aging Project (aged 79±8, 74% female). MEASUREMENTS: Baseline data on multiple life course factors included early-, mid-, and late-life participation in cognitive activities; early-life and adult SES; education; and reading ability (National Adult Reading Test; NART). Path analysis quantified direct and indirect standardized effects of life course factors on global cognition and five cognitive domains (episodic memory, semantic memory, working memory, visuospatial ability, perceptual speed). RESULTS: Adjusting for age, sex, and race, education had the strongest association with global cognition, episodic memory, semantic memory, and visuospatial ability, whereas NART (followed by education) had the strongest association with working memory. Late-life cognitive activities had the strongest association with perceptual speed, followed by education. CONCLUSIONS: These cross-sectional findings suggest that education and reading ability are the most-robust proxy measures of cognitive reserve in relation to late-life cognition. Additional research leveraging path analysis is warranted to better understand how these life course factors, reflecting the latent construct of cognitive reserve, affect abnormal cognitive aging.

We hypothesized that patterns of elevated stroke mortality among those born in the US Stroke Belt (SB) states also prevailed for mortality related to all-cause dementia or Alzheimer Disease (AD). Cause specific mortality (contributing cause of death, including underlying cause cases) rates in 2000 for US-born African-Americans and whites aged 65–89 were calculated by linking national mortality records with population data based on race, sex, age, and birth state or state of residence in 2000. Birth in a SB state (North Carolina, South Carolina, Georgia, Tennessee, Arkansas, Mississippi, or Alabama) was cross-classified against SB residence at the 2000 Census. Compared to those who were not born in the SB, odds of all cause dementia mortality were significantly elevated by 29% for African-Americans and 19% for whites born in the SB. These patterns prevailed among individuals who no longer lived in the SB at death. Patterns were similar for AD-related mortality. Some non-SB states were also associated with significant elevations in dementia-related mortality. Dementia mortality rates follow geographic patterns similar to stroke mortality, with elevated rates among those born in the SB. This suggests important roles for geographically patterned childhood exposures in establishing cognitive reserve.

The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia. The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available. We present criteria for all-cause dementia and for AD dementia. We retained the general framework of probable AD dementia from the 1984 criteria. On the basis of the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis. We also retained the term possible AD dementia, but redefined it in a manner more focused than before. Biomarker evidence was also integrated into the diagnostic formulations for probable and possible AD dementia for use in research settings. The core clinical criteria for AD dementia will continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much work lies ahead for validating the biomarker diagnosis of AD dementia. © 2011 The Alzheimer's Association. All rights reserved.

Population studies strive to determine the prevalence of Alzheimer dementia but prevalence estimates vary widely. The challenges faced by several noted population studies for Alzheimer dementia in operationalizing current clinical diagnostic criteria for Alzheimer’s disease (AD) are 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 are 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 also could facilitate studies of the interactions of various forms of neurodegenerative disorders with cerebrovascular disease, resulting in “mixed dementia”.

ObjectiveThis investigation aimed at examining whether circulating inflammatory biomarkers C-reactive protein (CRP), interleukin-6 (IL6), and alpha 1-antichymotrypsin (ACT) were related to cerebrovascular disease (CVD) assessed by MRI.MethodsThe study included nondemented elderly participants of a community-based, multiethnic cohort, who received baseline MRI scans and had CRP (n = 508), ACT (435), and IL6 (N = 357) measured by ELISA. Silent brain infarcts and white matter hyperintensities (WMH) were derived from all available MRI scans at baseline, approximately 4.4 years after blood sample collection for inflammatory biomarkers. Repeated assessments of infarcts and WMH, as well as microbleeds assessment, were performed at follow-up MRI visits around 4.5 years later. Cross-sectional and longitudinal relationship between inflammatory biomarkers and CVD were analyzed using appropriate logistic regression models, generalized linear models, or COX models.ResultsAfter adjusting for age, sex, ethnicity, education, APOE genotype, and intracranial volume, 1 SD increase in log10IL6 was associated with infarcts on MRI {odds ratio [OR] (95% confidence interval [CI]) = 1.28 [1.02–1.60], p = 0.033}, and 1 SD increase in log10CRP and log10ACT was associated with microbleeds (OR [95% CI] = 1.46 [1.02–2.09], p = 0.041; and 1.65 [1.11–2.46], p = 0.013; respectively). One SD increase in log10ACT was also associated with larger WMH at the follow-up MRI (b = 0.103, p = 0.012) and increased accumulation of WMH volume (b = 0.062, p = 0.041) during follow-up. The associations remained significant after additional adjustment of vascular risk factors and excluding participants with clinical stroke.ConclusionsAmong older adults, increased circulating inflammatory biomarkers were associated with the presence of infarcts and microbleeds, WMH burden, and progression of WMH.

Social support may be important for cognitive aging, but studies incorporating life course data are rare. Latent growth curve models estimated 10-year cognitive trajectories in 9,538 participants (baseline ages 45–94; mean=64) in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) project. Retrospective report of greater childhood social support was associated with better initial episodic memory (standardized estimate=0.08; 95% CI=0.05–0.10) and verbal fluency (standardized estimate=0.05; 95% CI=0.03–0.07), but not with subsequent rates of cognitive decline. Childhood social support effects on initial cognition were larger than or similar to independent effects of self-reported parental education. Effects were partially or fully mediated by higher education, lower body mass index, less perceived stress, and fewer depressive symptoms later in life. Childhood social support was more strongly associated with memory in Black participants, compared with White participants. These results suggest broad and enduring effects of childhood social support across the life course.

The 2008 Diversity Summit recognized the many advantages of increasing the number of neuropsychologists from ethnically diverse backgrounds. The Summit addressed the aspiration of creating a more ethnically diverse body of neuropsychologists by increasing the recruitment of ethnic minority students to neuropsychology training programs. Challenges to successful recruitment and retention of ethnic minority students were discussion points at the Summit. This paper summarizes and expands these points and also suggests solutions to these challenges with the aim of stimulating innovative approaches to increasing the representation of ethnic minorities in neuropsychology.

Importance The high prevalence of hypertension among the US black population is a major contributor to disparities in life expectancy; however, the causes for higher incidence of hypertension among black adults are unknown. Objective To evaluate potential factors associated with higher risk of incident hypertension among black adults. Design, Setting, and Participants Prospective cohort study of black and white adults selected from a longitudinal cohort study of 30 239 participants as not having hypertension at baseline (2003-2007) and participating in a follow-up visit 9.4 years (median) later. Exposures There were 12 clinical and social factors, including score for the Southern diet (range, −4.5 to 8.2; higher values reflect higher level of adherence to the dietary pattern), including higher fried and related food intake. Main Outcomes and Measures Incident hypertension (systolic blood pressure ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or use of antihypertensive medications) at the follow-up visit. Results Of 6897 participants (mean [SD] age, 62 [8] years; 26% were black adults; and 55% were women), 46% of black participants and 33% of white participants developed hypertension. Black men had an adjusted mean Southern diet score of 0.81 (95% CI, 0.72 to 0.90); white men, −0.26 (95% CI, −0.31 to −0.21); black women, 0.27 (95% CI, 0.20 to 0.33); and white women, −0.57 (95% CI, −0.61 to −0.54). The Southern diet score was significantly associated with incident hypertension for men (odds ratio [OR], 1.16 per 1 SD [95% CI, 1.06 to 1.27]; incidence of 32.4% at the 25th percentile and 36.1% at the 75th percentile; difference, 3.7% [95% CI, 1.4% to 6.2%]) and women (OR, 1.17 per 1 SD [95% CI, 1.08 to 1.28]; incidence of 31.0% at the 25th percentile and 34.8% at the 75th percentile; difference, 3.8% [95% CI, 1.5% to 5.8%]). The Southern dietary pattern was the largest mediating factor for differences in the incidence of hypertension, accounting for 51.6% (95% CI, 18.8% to 84.4%) of the excess risk among black men and 29.2% (95% CI, 13.4% to 44.9%) of the excess risk among black women. Among black men, a higher dietary ratio of sodium to potassium and an education level of high school graduate or less each mediated 12.3% of the excess risk of incident hypertension. Among black women, higher body mass index mediated 18.3% of the excess risk; a larger waist, 15.2%; less adherence to the Dietary Approaches to Stop Hypertension diet, 11.2%; income level of $35 000 or less, 9.3%; higher dietary ratio of sodium to potassium, 6.8%; and an education level of high school graduate or less, 4.1%. Conclusions and Relevance In a mediation analysis comparing incident hypertension among black adults vs white adults in the United States, key factors statistically mediating the racial difference for both men and women included Southern diet score, dietary ratio of sodium to potassium, and education level. Among women, waist circumference and body mass index also were key factors.

OBJECTIVE: The purpose of this study was to examine whether neuropsychological tests translated into Spanish measure the same cognitive constructs as the original English versions. METHOD: Older adult participants (N = 2,664), who did not exhibit dementia from the Washington Heights Inwood Columbia Aging Project (WHICAP), a community-based cohort from northern Manhattan, were evaluated with a comprehensive neuropsychological battery. The study cohort includes both English (n = 1,800) and Spanish speakers (n = 864) evaluated in their language of preference. Invariance analyses were conducted across language groups on a structural equation model comprising four neuropsychological factors (memory, language, visual-spatial ability, and processing speed). RESULTS: The results of the analyses indicated that the four-factor model exhibited partial measurement invariance, demonstrated by invariant factor structure and factor loadings but nonequivalent observed score intercepts. CONCLUSION: The finding of invariant factor structure and factor loadings provides empirical evidence to support the implicit assumption that scores on neuropsychological tests are measuring equivalent psychological traits across these two language groups. At the structural level, the model exhibited invariant factor variances and covariances.

These proceedings document the Multicultural Problem Solving Summit, which was held in Waikoloa Village, Hawaii in February 2008. Welcoming comments were followed by a brief review of the history o...

Plasma Abeta42 and Abeta40 levels are putative biomarkers for Alzheimer's disease (AD), but their significance and predictive value have been inconclusive. In AD transgenic models, plasma and cerebrospinal fluid levels of Abeta42 and Abeta40 increase with age but subsequently decrease when Abeta begins to accumulate in brain and with the onset of cognitive impairment. To determine the predictive value of Abeta levels in elderly populations, we investigated how plasma Abeta42, Abeta40, and a protofibrillar subspecies of Abeta42 changed over time and with the onset of cognitive impairment or AD. In a cohort of 1,125 elderly persons without dementia, 104 (9.2%) of the participants developed AD over 4.6 years of follow-up. Higher plasma Abeta42 levels at the onset of the study were associated with a threefold increased risk of AD. However, conversion to AD was accompanied by a significant decline in plasma Abeta42, a decreased Abeta42/Abeta40 ratio and, with the onset of cognitive impairment, decreased protofibrillar Abeta42 levels. Our results suggest individuals with elevated plasma Abeta42 are at increased risk of AD and that with the onset of disease, the decline in some forms of Abeta may reflect compartmentalization of Abeta peptides in the brain.

There is widespread agreement that many neuropsychological measures do not have acceptable diagnostic accuracy when used among people who are not Caucasian, welleducated, native English-speaking, and middle to upper class (Ardila et al. 2002; Boone et al. 2007; Brickman et al. 2006; Loewenstein et al. 1994; Manly 2005). A review of scholarly works reveals that not only is this an area of controversy in our field, but also that neuropsychological testing among culturally and linguistically diverse people is an area of critical vulnerability in the theoretical and empirical foundation for neuropsychological practice. The current status of neuropsychological practice among culturally and linguistically diverse people raises ethical questions. Guidelines for ethical decision-making within the neuropsychological assessment of ethnically and linguistically diverse people has been discussed in detail in several prior publications (Artiola i Fortuny & Mullaney 1997; Brickman et al. 2006; Harris et al. 2002; Wong 2006), making ethics one of the more comprehensively documented “subtopics” in cultural neuropsychology. The American Psychological Association Ethics Code (“Ethical Principles of Psychologists and Code of Conduct” 2002) states that it is unethical to use inappropriate measures among culturally different individuals. Yet, refusing to assess a large and growing segment of the population, many of whom may potentially benefit from neuropsychological services, would also violate the ethics of our field (Brickman et al. 2006; Harris et al. 2002). It is our ethical obligation to safeguard the welfare of people who come under our care, to take cultural background into account and to do our best to eliminate bias (“Ethical Principles of Psychologists and Code of Conduct” 2002). The quality and accuracy of current assessment of culturally diverse people may be “the very best we can do” but whether this level of practice is justified entirely depends on the setting of the assessment, what is at stake, the evidence base for the methods used, and the level of cultural competency of the neuropsychologist. Despite recent proliferation in the number of publications that directly address ethical, theoretical, and practical issues in cultural neuropsychology, the explosive growth in the number of culturally and linguistically diverse people in the United States has exposed our lack of preparation. We are playing a game of catch-up that is, in part, responsive to the pressure of a national research agenda of reducing health disparities in the United States. Cognitive function has been implicated as a critical predictor and outcome of gaps in health across the lifecourse (see Glymour and Manly, this issue), and therefore accurate assessment is crucial in addressing these disparities. The facts on America’s growing cultural diversity are essential knowledge for neuropsychologists in the in the United States. Although 66% of the population is nonHispanic White in 2008, this “majority” group will contribute far less of the total population growth in coming years. The non-Hispanic White share of the U.S. population has fallen steadily from 74% in 1995 to 66 percent in 2008, Neuropsychol Rev (2008) 18:179–183 DOI 10.1007/s11065-008-9068-8

Accurate neuropsychological assessment of older individuals from heterogeneous backgrounds is a major challenge. Education, ethnicity, language, and age are associated with scale level differences in test scores, but item level bias might contribute to these differences. We evaluated several strategies for dealing with item and scale level demographic influences on a measure of executive abilities defined by working memory and fluency tasks. We determined the impact of differential item functioning (DIF). We compared composite scoring strategies on the basis of their relationships with volumetric magnetic resonance imaging (MRI) measures of brain structure. Participants were 791 Hispanic, white, and African American older adults. DIF had a salient impact on test scores for 9% of the sample. MRI data were available on a subset of 153 participants. Validity in comparison with structural MRI was higher after scale level adjustment for education, ethnicity/language, and gender, but item level adjustment did not have a major impact on validity. Age adjustment at the scale level had a negative impact on relationships with MRI, most likely because age adjustment removes variance related to age-associated diseases. (JINS, 2008,14, 746–759.)