Education Does Not Affect Cognitive Decline in Aging: A Bayesian Assessment of the Association Between Education and Change in Cognitive Performance.
Ontology highlight
ABSTRACT:
SUBMITTER: Berggren R
PROVIDER: S-EPMC6043857 | biostudies-literature | 2018
REPOSITORIES: biostudies-literature
Publications
Education Does Not Affect Cognitive Decline in Aging: A Bayesian Assessment of the Association Between Education and Change in Cognitive Performance.
Berggren Rasmus R Nilsson Jonna J Lövdén Martin M
Frontiers in psychology 20180706
Education is positively associated with level of cognitive function but the association between education and rate of cognitive decline remains unresolved, partly for methodological reasons. In this article, we address this issue using linear mixed models and Bayesian hypothesis testing, using data from the Betula cohort-sequential longitudinal study. Our results support the null hypothesis that education does not alter the rate of cognitive decline for visuospatial ability, semantic knowledge, ...[more]
Similar Datasets
Project description:BackgroundThe objective of this study was to examine the association between education and incidence of accelerated cognitive decline.MethodsSecondary analyses of data from the Health and Retirement Study (HRS), a nationally representative prospective cohort study of U.S. residents were conducted (N = 28,417). Cox proportional hazards survival models were layered on longitudinal mixed-effects modeling to jointly examine healthy cognitive aging and incidence of accelerated cognitive decline consistent with patterns seen in preclinical Alzheimer's disease and related dementias (ADRD). Replication analyses were completed on a database including 62,485 additional respondents from HRS sister studies. Life expectancy ratios (LER) and 95% confidence intervals (CIs) were reported.ResultsThis study replicated research showing that education was positively associated with cognition at baseline. Model fit improved using the survival method compared to random-slopes models alone. Analyses of HRS data revealed that higher education was associated with delayed onset of accelerated cognitive decline (LER = 1.031 95% CI = [1.013-1.015], p < 1E-06). Replication analyses using data from 14 countries identified similar results.ConclusionsThese results are consistent with cognitive reserve theory, suggesting that education reduces risk of ADRD-pattern cognitive decline. Follow-up work should seek to differentiate specific dementia types involved and consider potential mechanisms.
| S-EPMC7424268 | biostudies-literature
Project description:BackgroundAlthough not strongly correlated with current objective cognitive ability, subjective cognitive decline (SCD) is a risk factor for Alzheimer's disease. Most studies focus on SCD in relation to future decline rather than objective prior decline that it purportedly measures.ObjectiveWe evaluated whether self-report of cognitive decline-as a continuous measure-corresponds to objectively-assessed episodic memory and executive function decline across the same period.Methods1,170 men completed the Everyday Cognition Questionnaire (ECog) at mean age 68 assessing subjective changes in cognitive ability relative to 10 years prior. A subset had mild cognitive impairment (MCI), but MCI was diagnosed without regard to subjective decline. Participants completed up to 3 objective assessments of memory and executive function (M = 56, 62, and 68 years). Informant-reported ECogs were completed for 1,045 individuals. Analyses controlled for depression and anxiety symptoms assessed at mean age 68.ResultsParticipant-reported ECog scores were modestly associated with objective decline for memory (β= -0.23, 95%CI [-0.37, -0.10]) and executive function (β= -0.19, 95%CI [-0.33, -0.05]) over the same time period. However, these associations were nonsignificant after excluding MCI cases. Results were similar for informant ratings. Participant-rated ECog scores were more strongly associated with concurrent depression and anxiety symptoms, (β= 0.44, 95%CI [0.36, 0.53]).ConclusionContinuous SCD scores are correlated with prior objective cognitive changes in non-demented individuals, though this association appears driven by individuals with current MCI. However, participants' current depression and anxiety ratings tend to be strongly associated with their SCD ratings. Thus, what primarily drives SCD ratings remains unclear.
| S-EPMC8482061 | biostudies-literature
Project description:This study (n=161) related morphometric MR imaging, FDG-PET and APOE genotype to memory scores in normal controls (NC), mild cognitive impairment (MCI) and Alzheimer's disease (AD). Stepwise regression analyses focused on morphometric and metabolic characteristics of the episodic memory network: hippocampus, entorhinal, parahippocampal, retrosplenial, posterior cingulate, precuneus, inferior parietal, and lateral orbitofrontal cortices. In NC, hippocampal metabolism predicted learning; entorhinal metabolism predicted recognition; and hippocampal metabolism predicted recall. In MCI, thickness of the entorhinal and precuneus cortices predicted learning, while parahippocampal metabolism predicted recognition. In AD, posterior cingulate cortical thickness predicted learning, while APOE genotype predicted recognition. In the total sample, hippocampal volume and metabolism, cortical thickness of the precuneus, and inferior parietal metabolism predicted learning; hippocampal volume and metabolism, parahippocampal thickness and APOE genotype predicted recognition. Imaging methods appear complementary and differentially sensitive to memory in health and disease. Medial temporal and parietal metabolism and morphometry best explained memory variance. Medial temporal characteristics were related to learning, recall and recognition, while parietal structures only predicted learning.
| S-EPMC3947581 | biostudies-literature
Project description:ObjectivesIn healthy aging, the way people cope differently with cognitive and neural decline is influenced by exposure to cognitively enriching life-experiences. Education is one of them, so that in general, the higher the education, the better the expected cognitive performance in aging. At the neural level, it is not clear yet how education can differentiate resting state functional connectivity profiles and their cognitive underpinnings. Thus, with this study, we aimed to investigate whether the variable education allowed for a finer description of age-related differences in cognition and resting state FC.MethodsWe analyzed in 197 healthy individuals (137 young adults aged 20-35 and 60 older adults aged 55-80 from the publicly available LEMON database), a pool of cognitive and neural variables, derived from magnetic resonance imaging, in relation to education. Firstly, we assessed age-related differences, by comparing young and older adults. Then, we investigated the possible role of education in outlining such differences, by splitting the group of older adults based on their education.ResultsIn terms of cognitive performance, older adults with higher education and young adults were comparable in language and executive functions. Interestingly, they had a wider vocabulary compared to young adults and older adults with lower education. Concerning functional connectivity, the results showed significant age- and education-related differences within three networks: the Visual-Medial, the Dorsal Attentional, and the Default Mode network (DMN). For the DMN, we also found a relationship with memory performance, which strengthen the evidence that this network has a specific role in linking cognitive maintenance and FC at rest in healthy aging.DiscussionOur study revealed that education contributes to differentiating cognitive and neural profiles in healthy older adults. Also, the DMN could be a key network in this context, as it may reflect some compensatory mechanisms relative to memory capacities in older adults with higher education.
| S-EPMC10244540 | biostudies-literature
Project description:Apolipoprotein E (APOE) is an important risk factor for cognitive decline and Alzheimer's disease in aging individuals. Among the 3 known alleles of this gene: e2, e3, and e4, the e4 allele is associated with faster cognitive decline and increased risk for Alzheimer's and dementia, while the e2 allele has a positive effect on longevity, and possibly on preservation of cognitive function. Education also has an important effect on cognition and longevity but the interplay between APOE and education is not well-characterized. Previous studies of the effect of APOE on cognitive decline often used linear regression with the normality assumption, which may not be appropriate for analyzing bounded and skewed neuropsychological test scores. In this paper, we applied Bayesian beta regression to assess the effect of APOE alleles on cognitive decline in a cohort of centenarians with longitudinal assessment of their cognitive function. The analysis confirmed the negative association between older age and cognition and the beneficial effect of education that persists even at the extreme of human lifespan in carriers of the e3 allele. In addition, the analysis showed an association between APOE and cognition that is modified by education. Surprisingly, an antagonistic interaction existed between higher education and APOE alleles, suggesting that education may reduce the positive effect of APOE e2 and increase the negative effect of APOE e4 at extreme old age.
| S-EPMC7820893 | biostudies-literature
Project description:We conducted a randomized controlled trial to examine choral singing's effect on cognitive decline in aging. Older Singaporeans who were at high risk of future dementia were recruited: 47 were assigned to choral singing intervention (CSI) and 46 were assigned to health education program (HEP). Participants attended weekly one-hour choral singing or weekly one-hour health education for two years. Change in cognitive function was measured by a composite cognitive test score (CCTS) derived from raw scores of neuropsychological tests; biomarkers included brain magnetic resonance imaging, oxidative damage and immunosenescence. The average age of the participants were 70 years and 73/93 (78.5%) were female. The change of CCTS from baseline to 24 months was 0.05 among participants in the CSI group and -0.1 among participants in the HEP group. The between-group difference (0.15, p=0.042) became smaller (0.12, p=0.09) after adjusting for baseline CCTS. No between-group differences on biomarkers were observed. Our data support the role of choral singing in improving cognitive health in aging. The beneficial effect is at least comparable than that of health education in preventing cognitive decline in a community of elderly people. Biological mechanisms underlying the observed efficacy should be further studied.
| S-EPMC7803497 | biostudies-literature
Project description:Recent microarray studies in the hippocampus of rodents or Alzheimerâs disease (AD) subjects have identified a substantial number of cellular pathways/processes correlated with aging and cognitive decline. However, the temporal relationships among these expression changes or with cognitive impairment have not been studied in depth. Here, using Affymetrix microarrays, immunohistochemistry and Morris water maze cognitive testing across 5 age groups of male F344 rats (n=9-15/group, one microarray per animal), we systematically analyzed the temporal sequence and cellular localization of aging changes in expression. These were correlated with performance scores on the hippocampus-dependent Morris Water Maze task. Significant microarray results were sorted in to Early, Intermediate, Midlife, and Late patterns of expression, and functionally categorized (Early- downregulated neural development, lipid synthesis and energy-utilization; upregulated ribosomal synthesis, growth, stress/inflammatory, lysosome and protein/lipid degradation. Intermediate- increased defense/inflammatory activation and decreased transporter activity; Midlife- downregulated energy-dependent signaling and neurite growth, upregulated astroglial activation, Ca2+-binding, cholesterol/lipid trafficking, myelinogenic processes and additional lysosome/inflammation; Late- further recruitment of genes in already-altered pathways). Immunohistochemistry revealed a primarily astrocytic localization of the processes upregulated in midlife, as well as increased density of myelin proteins. Evidence of cognitive impairment first appeared in the 12-month-old group (midlife) and was increased further in the 23-month-old group, exhibiting the highest correlations with some upregulated genes related to cholesterol transport (e.g., Apoe, Abca2), protein management and ion binding. Some upregulated genes for inflammation (Il6st) and myelinogenesis (Pmp22) also correlated with impairment. Together, the data are consistent with a novel sequential cascade model of brain aging in which metabolic alterations early in maturity are followed by inflammation and midlife activation of an astrocyte-centered cholesterol trafficking pathway that stimulates oligodendrocyte remyelination programs. Importantly, this cholesterol trafficking pathway also may compete for astroglial bioenergetic support of neurons, in turn, leading to downregulation of energy-dependent pathways needed to sustain cognitive functions. Experiment Overall Design: Fisher 344 rats aged 3 (n = 9), 6 (n = 9), 9 (n = 9), 12 (n = 9), or 25 (n = 15; but see below) months were behaviorally characterized on the Morris water maze. Briefly, animals were placed in a circular water bath chamber with a partially submerged platform. Three times per day for three days, animals were placed at randomized starting points with the goal of locating the hidden platform. Generally, animals became better at locating the platform, and by the third day of training, were reliably swimming directly to the platform despite randomized starting loci. On the fourth day, the platform was removed and the degree to which the animals focused their searches on the area that previously contained the platform was measured. On the last day of behavior, animals were given a cue trial in which the platform was raised above the water level so that the rats could see it. Measures taken from the behavior study included path length (how long did the animal swim prior to locating the platform/ platform area), latency to platform in seconds, and velocity (centimeters/ second; swim speed). Two aged animals (E2 and E12) were removed from the study for poor health, reducing the 23 month cohort (n = 13). Twelve to twenty four hours after the last behavioral session, animals were killed and their hippocampi removed. The right hippocampus went to immunohistochemistry for quantification and localization of selected protein products. The left hippocampus was dissected, the CA1 region removed and frozen in dry ice prior to microarray processing. mRNA was extracted from each animal's tissue by standard Affymetrix protocols (see Blalock et al., 2003) and hybridized to individual microarrays (RAE 230A; N = 49 arrays in total). Results were processed with the MAS5 algorithm and subjected to âall probe setâ scaling with a target intensity of 500. Probe sets were filtered for presence (> = 5 presence calls study wide) and gene symbol level annotation prior to statistical analysis. 1-ANOVA across age was used to identify aging-related probe sets/genes (p <= 0.05). Aging-related genes were subjected to post hoc template correlation to determine the pattern of age-related change, and further, within the 12 and 23 month old groups, Pearson's correlation with behavioral scores was used to identify genes whose expression levels correlated significantly (p <= 0.05) with behavior. Twelve and 23 month old groups were chosen for this correlation analysis as they showed the greatest variability among similarly aged animals, suggesting that these ages show important cognitive transition phases during aging-related cognitive decline. Functional grouping analysis was performed using the DAVID suite of on-line tools.
2009-01-25 | E-GEOD-9990 | biostudies-arrayexpress
Project description:The goal of this study was to investigate the linkages of positive affect (PA) with cognitive health and its decline among elder Mexican Americans. We conducted secondary analysis of longitudinal data from the Sacramento Area Latino Study on Aging (SALSA). We used the structural equation modeling framework to achieve three specific aims: (1) identify a valid measure of PA, (2) describe within-person trajectories of PA and cognitive health, and (3) test the inter-relations of these two processes over time. Results showed that, on average, PA and cognitive ability (including verbal memory) decreased over time. Yet, there was significant variability in these patterns of change. Bivariate latent growth curve models showed significant correlations of baseline levels and rates of change of PA and cognitive ability even after controlling for age, education, sex, bilingualism, and depression. Results support the hypothesis that increases and decreases in PA tend to be related to increases and decreases in cognitive health at old age among Mexican Americans.
| S-EPMC6889886 | biostudies-literature
Project description:IntroductionEducational differences in cognitive performance among older adults are well documented. Studies that explore this association typically estimate a single average effect of education on cognitive performance. We argue that the processes that contribute to the association between education and cognitive performance are unlikely to have equal effects at all levels of cognitive performance. In this study, we employ an analytical approach that enables us to go beyond averages to examine the association between education and five measures of global and domain-specific cognitive performance across the outcome distributions.MethodsThis cross-sectional study included 1,780 older adults aged 58-68 years from the Longitudinal Aging Study Amsterdam. Conditional quantile regression was used to examine variation across the outcome distribution. Cognitive outcomes included Mini-Mental State Examination (MMSE) score, crystallized intelligence, information processing speed, episodic memory, and a composite score of global cognitive performance.ResultsThe results showed that the associations between education and different cognitive measures varied across the outcome distributions. Specifically, we found that education had a stronger association with crystallized intelligence, MMSE, and a composite cognitive performance measure in the lower tail of performance distributions. The associations between education and information processing speed and episodic memory were uniform across the outcome distributions.ConclusionLarger associations between education and some domains of cognitive performance in the lower tail of the performance distributions imply that inequalities are primarily generated among individuals with lower performance rather than among average and high performers. Additionally, the varying associations across some of the outcome distributions indicate that estimating a single average effect through standard regression methods may overlook variations in cognitive performance between educational groups. Future studies should consider heterogeneity across the outcome distribution.
| S-EPMC10911170 | biostudies-literature
Project description:Both social and genetic factors contribute to cognitive impairment and decline, yet genetic factors identified through genome-wide association studies (GWAS) explain only a small portion of trait variability. This "missing heritability" may be due to rare, potentially functional, genetic variants not assessed by GWAS, as well as gene-by-social factor interactions not explicitly modeled. Gene-by-social factor interactions may also operate differently across race/ethnic groups. We selected 39 genes that had significant, replicated associations with cognition, dementia, and related traits in published GWAS. Using gene-based analysis (SKAT/iSKAT), we tested whether common and/or rare variants were associated with episodic memory performance and decline either alone or through interaction with education in >10,000 European ancestry (EA) and >2200 African ancestry (AA) respondents from the Health and Retirement Study (HRS). Nine genes in EA and five genes in AA were associated with memory performance or decline (p < 0.05), and these effects did not attenuate after adjusting for education. Interaction between education and CLPTM1 on memory performance was significant in AA (p = 0.003; FDR-adjusted p = 0.038) and nominally significant in EA (p = 0.026). In both ethnicities, low memory performance was associated with CLPTM1 genotype (rs10416261) only for those with less than high school education, and effects persisted after adjusting for APOE ε4. For over 70% of gene-by-education interactions across the genome that were at least nominally significant in either ethnic group (p < 0.05), genetic effects were only observed for those with less than high school education. These results suggest that genetic effects on memory identified in this study are not mediated by education, but there may be important gene-by-education interactions across the genome, including in the broader APOE genomic region, which operate independently of APOE ε4. This work illustrates the importance of developing theoretical frameworks and methodological approaches for integrating social and genomic data to study cognition across ethnic groups.
| S-EPMC6510651 | biostudies-literature