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      Associations between social relationship measures, serum brain-derived neurotrophic factor, and risk of stroke and dementia

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          Abstract

          Introduction

          Mechanisms underlying social determinants of stroke and dementia are unclear and brain-derived neurotrophic factor (BDNF) may contribute as a molecular link.

          Methods

          Using the Framingham Study, we examined social relationship measures as predictors of higher serum BDNF level and cumulative incidence of stroke and dementia.

          Results

          Among 3294 participants, controlling for age and sex, isolation trended with lower BDNF (odds ratio = 0.69 [0.47–1.00]). Participants with more companionship had reduced risk for stroke (hazard ratio [HR] = 0.59 [0.41–0.83]) and dementia (HR = 0.67 [0.49–0.92]). Greater emotional support was associated with higher BDNF (odds ratio = 1.27 [1.04–1.54]), reduced dementia risk (HR = 0.69 [0.51–0.94], and among smokers, reduced stroke risk (HR = 0.23 [0.10–0.57]). Associations persisted after additional adjustments. BDNF partly mediated the total effect between emotional support and dementia risk.

          Conclusions

          Availability of social support appears to be associated with increased BDNF levels and, in certain subsets, reduce risk of subsequent dementia and stroke, thus warranting study of these pathways to understand their role in neuroprotection.

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          Most cited references 24

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          From social integration to health: Durkheim in the new millennium.

          It is widely recognized that social relationships and affiliation have powerful effects on physical and mental health. When investigators write about the impact of social relationships on health, many terms are used loosely and interchangeably including social networks, social ties and social integration. The aim of this paper is to clarify these terms using a single framework. We discuss: (1) theoretical orientations from diverse disciplines which we believe are fundamental to advancing research in this area; (2) a set of definitions accompanied by major assessment tools; and (3) an overarching model which integrates multilevel phenomena. Theoretical orientations that we draw upon were developed by Durkheim whose work on social integration and suicide are seminal and John Bowlby, a psychiatrist who developed attachment theory in relation to child development and contemporary social network theorists. We present a conceptual model of how social networks impact health. We envision a cascading causal process beginning with the macro-social to psychobiological processes that are dynamically linked together to form the processes by which social integration effects health. We start by embedding social networks in a larger social and cultural context in which upstream forces are seen to condition network structure. Serious consideration of the larger macro-social context in which networks form and are sustained has been lacking in all but a small number of studies and is almost completely absent in studies of social network influences on health. We then move downstream to understand the influences network structure and function have on social and interpersonal behavior. We argue that networks operate at the behavioral level through four primary pathways: (1) provision of social support; (2) social influence; (3) on social engagement and attachment; and (4) access to resources and material goods.
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            Exercise and brain neurotrophins.

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              Probability of stroke: a risk profile from the Framingham Study.

              A health risk appraisal function has been developed for the prediction of stroke using the Framingham Study cohort. The stroke risk factors included in the profile are age, systolic blood pressure, the use of antihypertensive therapy, diabetes mellitus, cigarette smoking, prior cardiovascular disease (coronary heart disease, cardiac failure, or intermittent claudication), atrial fibrillation, and left ventricular hypertrophy by electrocardiogram. Based on 472 stroke events occurring during 10 years' follow-up from biennial examinations 9 and 14, stroke probabilities were computed using the Cox proportional hazards model for each sex based on a point system. On the basis of the risk factors in the profile, which can be readily determined on routine physical examination in a physician's office, stroke risk can be estimated. An individual's risk can be related to the average risk of stroke for persons of the same age and sex. The information that one's risk of stroke is several times higher than average may provide the impetus for risk factor modification. It may also help to identify persons at substantially increased stroke risk resulting from borderline levels of multiple risk factors such as those with mild or borderline hypertension and facilitate multifactorial risk factor modification.
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                Author and article information

                Contributors
                Journal
                Alzheimers Dement (N Y)
                Alzheimers Dement (N Y)
                Alzheimer's & Dementia : Translational Research & Clinical Interventions
                Elsevier
                2352-8737
                22 March 2017
                June 2017
                22 March 2017
                : 3
                : 2
                : 229-237
                Affiliations
                [a ]Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
                [b ]The Framingham Heart Study, Boston, MA, USA
                [c ]Department of Epidemiology, Harvard Center for Population and Development Studies, Harvard TH Chan School of Public Health, Boston, MA, USA
                [d ]Department of Social and Behavioral Sciences, Harvard Center for Population and Development Studies, Harvard TH Chan School of Public Health, Boston, MA, USA
                [e ]Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA
                [f ]Department of Neurology, Boston University School of Medicine, Boston, MA, USA
                [g ]School of Public Health, University of Haifa, Haifa, Israel
                [h ]Center for Human Genetics Research, Massachusetts General Hospital, Boston, MA, USA
                Author notes
                []Corresponding author. Tel.: +1-617-726-4881; Fax: +1-617-724-7836. joelsalinas@ 123456mail.harvard.edu
                Article
                S2352-8737(17)30012-4
                10.1016/j.trci.2017.03.001
                5651441
                © 2017 The Authors

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

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