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      Educational inequalities in aging-related declines in fluid cognition and the onset of cognitive pathology

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          Abstract

          Background

          Education has been robustly associated with cognitive reserve and dementia, but not with the rate of cognitive aging, resulting in some confusion about the mechanisms of cognitive aging. This study uses longitudinal data to differentiate between trajectories indicative of healthy versus pathologic cognitive aging.

          Methods

          Participants included 9401 Health and Retirement Study respondents aged ≥55 years who completed cognitive testing regularly over 17.3 years until most recently in 2012. Individual-specific random change-point modeling was used to identify age of incident pathologic decline; acceleration is interpreted as indicating likely onset of pathologic decline when it is significant and negative.

          Results

          These methods detect incident dementia diagnoses with specificity/sensitivity of 89.3%/44.3%, 5.6 years before diagnosis. Each year of education was associated with 0.09 (95% confidence interval [CI], 0.087–0.096; P < .001) standard deviation higher baseline cognition and delayed onset of cognitive pathology (hazard ratio, 0.98; 95% CI, 0.96–0.99; P = .006).

          Conclusions

          Longitudinal random change-point modeling was able to reliably identify incident dementia. Accounting for incident cognitive pathology, we find that education predicts cognitive capability and delayed onset pathologic declines.

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          Most cited references55

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          A Proportional Hazards Model for the Subdistribution of a Competing Risk

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            Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade.

            Currently available evidence strongly supports the position that the initiating event in Alzheimer's disease (AD) is related to abnormal processing of beta-amyloid (Abeta) peptide, ultimately leading to formation of Abeta plaques in the brain. This process occurs while individuals are still cognitively normal. Biomarkers of brain beta-amyloidosis are reductions in CSF Abeta(42) and increased amyloid PET tracer retention. After a lag period, which varies from patient to patient, neuronal dysfunction and neurodegeneration become the dominant pathological processes. Biomarkers of neuronal injury and neurodegeneration are increased CSF tau and structural MRI measures of cerebral atrophy. Neurodegeneration is accompanied by synaptic dysfunction, which is indicated by decreased fluorodeoxyglucose uptake on PET. We propose a model that relates disease stage to AD biomarkers in which Abeta biomarkers become abnormal first, before neurodegenerative biomarkers and cognitive symptoms, and neurodegenerative biomarkers become abnormal later, and correlate with clinical symptom severity. Copyright 2010 Elsevier Ltd. All rights reserved.
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              Cognitive reserve in ageing and Alzheimer's disease.

              The concept of cognitive reserve provides an explanation for differences between individuals in susceptibility to age-related brain changes or pathology related to Alzheimer's disease, whereby some people can tolerate more of these changes than others and maintain function. Epidemiological studies suggest that lifelong experiences, including educational and occupational attainment, and leisure activities in later life, can increase this reserve. For example, the risk of developing Alzheimer's disease is reduced in individuals with higher educational or occupational attainment. Reserve can conveniently be divided into two types: brain reserve, which refers to differences in the brain structure that may increase tolerance to pathology, and cognitive reserve, which refers to differences between individuals in how tasks are performed that might enable some people to be more resilient to brain changes than others. Greater understanding of the concept of cognitive reserve could lead to interventions to slow cognitive ageing or reduce the risk of dementia. Copyright © 2012 Elsevier Ltd. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Alzheimers Dement (Amst)
                Alzheimers Dement (Amst)
                Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring
                Elsevier
                2352-8729
                28 June 2015
                September 2015
                28 June 2015
                : 1
                : 3
                : 303-310
                Affiliations
                [a ]Program in Public Health and Department of Preventive Medicine, Stony Brook University, Stony Brook, NY, USA
                [b ]Department of Epidemiology & Biostatistics, University of California, San Francisco, CA, USA
                [c ]MRC Unit for Lifelong Health and Ageing, University College London, London, UK
                Author notes
                []Corresponding author. Tel.: +1-631-444-6593; Fax: +1-631-444-3480. sean.clouston@ 123456stonybrookmedicine.edu
                Article
                S2352-8729(15)00052-4
                10.1016/j.dadm.2015.06.001
                4542007
                26309906
                4302f7c9-29fb-4a82-b1bb-1081d9f3aaaa
                © 2015 The Authors

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Categories
                Cognitive & Behavioral Assessment

                dementia,aging,neurology,social medicine,cognitive reserve,educational status

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