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      Education and Cognitive Functioning Across the Life Span

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          Abstract

          Cognitive abilities are important predictors of educational and occupational performance, socioeconomic attainment, health, and longevity. Declines in cognitive abilities are linked to impairments in older adults’ everyday functions, but people differ from one another in their rates of cognitive decline over the course of adulthood and old age. Hence, identifying factors that protect against compromised late-life cognition is of great societal interest. The number of years of formal education completed by individuals is positively correlated with their cognitive function throughout adulthood and predicts lower risk of dementia late in life. These observations have led to the propositions that prolonging education might (a) affect cognitive ability and (b) attenuate aging-associated declines in cognition. We evaluate these propositions by reviewing the literature on educational attainment and cognitive aging, including recent analyses of data harmonized across multiple longitudinal cohort studies and related meta-analyses. In line with the first proposition, the evidence indicates that educational attainment has positive effects on cognitive function. We also find evidence that cognitive abilities are associated with selection into longer durations of education and that there are common factors (e.g., parental socioeconomic resources) that affect both educational attainment and cognitive development. There is likely reciprocal interplay among these factors, and among cognitive abilities, during development. Education–cognitive ability associations are apparent across the entire adult life span and across the full range of education levels, including (to some degree) tertiary education. However, contrary to the second proposition, we find that associations between education and aging-associated cognitive declines are negligible and that a threshold model of dementia can account for the association between educational attainment and late-life dementia risk. We conclude that educational attainment exerts its influences on late-life cognitive function primarily by contributing to individual differences in cognitive skills that emerge in early adulthood but persist into older age. We also note that the widespread absence of educational influences on rates of cognitive decline puts constraints on theoretical notions of cognitive aging, such as the concepts of cognitive reserve and brain maintenance. Improving the conditions that shape development during the first decades of life carries great potential for improving cognitive ability in early adulthood and for reducing public-health burdens related to cognitive aging and dementia.

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          Hemispheric asymmetry reduction in older adults: the HAROLD model.

          A model of the effects of aging on brain activity during cognitive performance is introduced. The model is called HAROLD (hemispheric asymmetry reduction in older adults), and it states that, under similar circumstances, prefrontal activity during cognitive performances tends to be less lateralized in older adults than in younger adults. The model is supported by functional neuroimaging and other evidence in the domains of episodic memory, semantic memory, working memory, perception, and inhibitory control. Age-related hemispheric asymmetry reductions may have a compensatory function or they may reflect a dedifferentiation process. They may have a cognitive or neural origin, and they may reflect regional or network mechanisms. The HAROLD model is a cognitive neuroscience model that integrates ideas and findings from psychology and neuroscience of aging.
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            Intelligence and socioeconomic success: A meta-analytic review of longitudinal research

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              GWAS on family history of Alzheimer’s disease

              Alzheimer’s disease (AD) is a public health priority for the 21st century. Risk reduction currently revolves around lifestyle changes with much research trying to elucidate the biological underpinnings. We show that self-report of parental history of Alzheimer’s dementia for case ascertainment in a genome-wide association study of 314,278 participants from UK Biobank (27,696 maternal cases, 14,338 paternal cases) is a valid proxy for an AD genetic study. After meta-analysing with published consortium data (n = 74,046 with 25,580 cases across the discovery and replication analyses), three new AD-associated loci (P < 5 × 10−8) are identified. These contain genes relevant for AD and neurodegeneration: ADAM10, BCKDK/KAT8 and ACE. Novel gene-based loci include drug targets such as VKORC1 (warfarin dose). We report evidence that the association of SNPs in the TOMM40 gene with AD is potentially mediated by both gene expression and DNA methylation in the prefrontal cortex. However, it is likely that multiple variants are affecting the trait and gene methylation/expression. Our discovered loci may help to elucidate the biological mechanisms underlying AD and, as they contain genes that are drug targets for other diseases and disorders, warrant further exploration for potential precision medicine applications.
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                Author and article information

                Journal
                Psychol Sci Public Interest
                Psychol Sci Public Interest
                PSI
                sppsi
                Psychological Science in the Public Interest
                SAGE Publications (Sage CA: Los Angeles, CA )
                1529-1006
                2160-0031
                10 August 2020
                August 2020
                : 21
                : 1
                : 6-41
                Affiliations
                [1 ]Aging Research Center, Department of Neurobiology, Care Sciences, and Society, Karolinska Institutet and Stockholm University, Stockholm, Sweden
                [2 ]Department of Psychology, University of Gothenburg, Gothenburg, Sweden
                [3 ]Stockholm Gerontology Research Center, Stockholm, Sweden
                [4 ]Department of Epidemiology and Biostatistics, University of California, San Francisco
                [5 ]Center for Lifespan Psychology, Max Planck Institute for Human Development, Berlin, Germany
                [6 ]Max Planck UCL Centre for Computational Psychiatry and Ageing Research, Berlin, Germany, and London, United Kingdom
                [7 ]Department of Psychology and Population Research Center, University of Texas at Austin
                Author notes
                [*]Martin Lövdén, Department of Psychology, University of Gothenburg, Haraldsgatan 1, 413 14 Gothenburg, Sweden. E-mail: martin.lovden@ 123456psy.gu.se
                Article
                10.1177_1529100620920576
                10.1177/1529100620920576
                7425377
                32772803
                80fef5d1-238d-48ea-aa75-7cddbde61938
                © The Author(s) 2020

                This article is distributed under the terms of the Creative Commons Attribution 4.0 License ( https://creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

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                educational attainment,cognitive ability,cognitive aging,life-span development,dementia

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