Kelsey D Biddle1, Federico d'Oleire Uquillas2, Heidi I L Jacobs3, Benjamin Zide4, Dylan R Kirn2, Dorene M Rentz5, Keith A Johnson6, Reisa A Sperling5, Nancy J Donovan7. 1. Division of Geriatric Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. 2. Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. 3. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; School for Mental Health and Neuroscience, Alzheimer Centre Limburg, Maastricht University, Maastricht, The Netherlands. 4. Division of Geriatric Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. 5. Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. 6. Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. 7. Division of Geriatric Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. Electronic address: njdonovan@partners.org.
Abstract
OBJECTIVE: Public health recommendations promote social engagement to reduce risk of cognitive decline and dementia. The objective of this study was to evaluate the longitudinal associations of social engagement and cognition in cognitively normal older adults with varying levels of neocortical amyloid-β, the Alzheimer's disease (AD) pathologic marker. METHODS: Two hundred seventeen men and women, age 63-89 underwent assessments for social engagement and cognitive performance at baseline and 3 years later using the Community Healthy Activities Model Program for Seniors questionnaire and the Preclinical Alzheimer Cognitive Composite (PACC). Amyloid-β was measured using Pittsburgh compound B-PET. Multivariable regression models estimated main and interactive effects of baseline social engagement and amyloid-β on cognitive change. Reciprocal models estimated main and interactive effects of baseline cognitive performance and amyloid-β on change in social engagement. RESULTS: Baseline social engagement was associated with PACC change as a modifier but not as a main effect. Lower baseline social engagement was associated with greater amyloid-β-related PACC decline, while higher baseline social engagement was associated with relative preservation of PACC scores (β = 0.05, p = 0.03). Reciprocally, lower baseline PACC score was associated with decline in social engagement score (β = 1.1, p = 0.02). This association was not modified by amyloid-β, and there was no direct association of amyloid-β with change in social engagement. CONCLUSIONS: Low social engagement may be a marker of neurocognitive vulnerability in older adults who are cognitively normal but have evidence of AD pathophysiologic change. Understanding changes in social engagement in older adults may lead to earlier diagnosis of AD and advances in evidence-based prevention and treatment.
OBJECTIVE: Public health recommendations promote social engagement to reduce risk of cognitive decline and dementia. The objective of this study was to evaluate the longitudinal associations of social engagement and cognition in cognitively normal older adults with varying levels of neocortical amyloid-β, the Alzheimer's disease (AD) pathologic marker. METHODS: Two hundred seventeen men and women, age 63-89 underwent assessments for social engagement and cognitive performance at baseline and 3 years later using the Community Healthy Activities Model Program for Seniors questionnaire and the Preclinical Alzheimer Cognitive Composite (PACC). Amyloid-β was measured using Pittsburgh compound B-PET. Multivariable regression models estimated main and interactive effects of baseline social engagement and amyloid-β on cognitive change. Reciprocal models estimated main and interactive effects of baseline cognitive performance and amyloid-β on change in social engagement. RESULTS: Baseline social engagement was associated with PACC change as a modifier but not as a main effect. Lower baseline social engagement was associated with greater amyloid-β-related PACC decline, while higher baseline social engagement was associated with relative preservation of PACC scores (β = 0.05, p = 0.03). Reciprocally, lower baseline PACC score was associated with decline in social engagement score (β = 1.1, p = 0.02). This association was not modified by amyloid-β, and there was no direct association of amyloid-β with change in social engagement. CONCLUSIONS: Low social engagement may be a marker of neurocognitive vulnerability in older adults who are cognitively normal but have evidence of AD pathophysiologic change. Understanding changes in social engagement in older adults may lead to earlier diagnosis of AD and advances in evidence-based prevention and treatment.
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