Impact of Differential Attrition on the Association of Education With Cognitive Change Over 20 Years of Follow-up: The ARIC Neurocognitive Study

Gottesman, Rebecca F.; Rawlings, Andreea M.; Sharrett, A. Richey; Albert, Marilyn; Alonso, Álvaro; Bandeen‐Roche, Karen; Coker, Laura H.; Coresh, Josef; Couper, David J.; Griswold, Michael; Heiss, Gerardo; Knopman, David S.; Patel, Mehul D.; Penman, Alan D.; Power, Melinda C.; Selnes, Ola A.; Schneider, Andrea L.C.; Wagenknecht, Lynne E.; Windham, B. Gwen; Wruck, Lisa; Mosley, Thomas H.

doi:10.1093/aje/kwu020

Cited by 101 publications

(115 citation statements)

References 28 publications

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“…However, we have not found evidence that early-life factors offer protection against cognitive decline in the LBCs or other studies (Shenkin et al 2009b;Tucker-Drob et al 2009;Zahodne et al 2011;Gottesman et al 2014;. That is, they might be associated with long-standing cognitive level, but possibly not with cognitive trajectory.…”

Section: Early-life and Demographic Factorscontrasting

confidence: 78%

Healthy cognitive ageing in the Lothian Birth Cohort studies: marginal gains not magic bullet

2017

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In the face of shifting demographics and an increase in human longevity, it is important to examine carefully what is known about cognitive ageing, and to identify and promote possibly malleable lifestyle and health-related factors that might mitigate age-associated cognitive decline. The Lothian Birth Cohorts of 1921 (LBC1921, n = 550) and 1936 (LBC1936, n = 1091) are longitudinal studies of cognitive and brain ageing based in Scotland. Childhood IQ data are available for these participants, who were recruited in later life and then followed up regularly. This overview summarises some of the main LBC findings to date, illustrating the possible genetic and environmental contributions to cognitive function (level and change) and brain imaging biomarkers in later life. Key associations include genetic variation, health and fitness, psychosocial and lifestyle factors, and aspects of the brain's structure. It addresses some key methodological issues such as confounding by early-life intelligence and social factors and emphasises areas requiring further investigation. Overall, the findings that have emerged from the LBC studies highlight that there are multiple correlates of cognitive ability level in later life, many of which have small effects, that there are as yet few reliable predictors of cognitive change, and that not all of the correlates have independent additive associations. The concept of marginal gains, whereby there might be a cumulative effect of small incremental improvements across a wide range of lifestyle and health-related factors, may offer a useful way to think about and promote a multivariate recipe for healthy cognitive and brain ageing.

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Section: Early-life and Demographic Factorscontrasting

confidence: 78%

Healthy cognitive ageing in the Lothian Birth Cohort studies: marginal gains not magic bullet

2017

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“…Further, our own work in ARIC has suggested that level of educational attainment does not influence rate of cognitive decline itself, but rather raises the absolute level of scores, a manifestation of cognitive reserve, and might delay the age at which an individual passes below a threshold and is diagnosed with dementia. 34 These florbetapir data support that hypothesis, suggesting that the effect of education on healthy brain aging may be via cognitive reserve rather than through direct changes in amyloid deposition. Our education-adjusted data do not suggest that the race differences observed are the effects of differences in education.…”

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confidence: 54%

The ARIC-PET amyloid imaging study

et al. 2016

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Objective: To evaluate differences in amyloid deposition in a community-based cohort without dementia by age, sex, race, education, and APOE e4 allele status. Methods:Recruited from the longitudinal Atherosclerosis Risk in Communities study, 329 participants without dementia, ages 67-88 years, were imaged using florbetapir PET at 3 US community sites (Washington County, Maryland; Forsyth County, North Carolina; and Jackson, Mississippi). Standardized uptake value ratios (SUVRs) were calculated; global cortical SUVR .1.2 was evaluated as the primary outcome. Age, race, sex, education level, and number of APOE e4 alleles were evaluated in multivariable models including vascular risk factors, brain white matter hyperintensity and total intracranial volume, and cognitive status.Results: A total of 141 of the participants (43%) were black. In multivariable models, odds of elevated SUVR was increased in participants with increasing age (odds ratio [OR] 1.63, 95% confidence interval [CI] 1.01-2.65 per 10 years of age) and black race (OR 2.08, 95% CI 1.23-3.51) but did not differ by educational level. Each e4 allele was associated with increased odds of elevated SUVR (OR 2.65, 95% CI 1.61-4.39).Conclusions: In this community-based cohort without dementia, florbetapir uptake is associated with older age and APOE genotype. Black race was associated with higher SUVR, after adjusting for demographics, vascular risk factors, cognitive status, white matter hyperintensity volume, and APOE genotype, with effect sizes nearing those seen for APOE e4. Replication of these findings is needed in other cohorts, and reasons for and consequences of these observed differences by race warrant further study. The prevailing hypothesis behind the pathophysiology of Alzheimer disease (AD) focuses on the accumulation of brain amyloid in b-amyloid (Ab) plaques as a critical mechanism. Use of PET ligands that bind to Ab allows for the evaluation of Ab in persons with or without clinical symptoms. Although a recent meta-analysis reported positive amyloid scans in 10% of healthy 50-to 90-year-old participants, and in 27% of similarly aged adults with mild cognitive impairment (MCI), 1 few studies in persons of European extraction 2,3 have evaluated patterns of Ab deposition using PET, and none in black participants, to our knowledge. Using Ab imaging in a biracial cohort would allow further exploration of racial disparities in dementia etiology.Dementia is more prevalent in blacks than in whites, 4-6 although AD-type neuropathologic findings are found on autopsy with equal prevalence in both groups. 7,8 Thus, a larger component

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“…The utility of this approach is demonstrated by previous findings in the ARIC Study that educational level, although strongly associated with cognitive performance at any single visit, is not an important predictor of cognitive change . 38,39 …”

Section: Discussionmentioning

confidence: 99%