Stephen F Smagula1, Lana Chahine2, Andrea Metti3, Anusha Rangarajan4, Howard J Aizenstein4, Qu Tian5, Caterina Rosano3. 1. Department of Psychiatry (SFS, AR, and HJA), School of Medicine, University of Pittsburgh, Pittsburgh, PA. Electronic address: sfs26@pitt.edu. 2. Department of Neurology (LC), School of Medicine, University of Pittsburgh, Pittsburgh, PA. 3. Department of Epidemiology (AM and CR), Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA. 4. Department of Psychiatry (SFS, AR, and HJA), School of Medicine, University of Pittsburgh, Pittsburgh, PA. 5. Intramural Research Program (QT), National Institute on Aging, Baltimore, MD.
Abstract
OBJECTIVES: We examined the extent to which measures of neurodegeneration and cerebrovascular disease explain the rest-activity rhythm (RAR)-cognition link. METHODS: Seventy participants (mean age at MRI = 86, standard deviation (SD) = 2.6; 53% female) had cognitive, MRI, and accelerometer data. The slope of cognitive decline was defined applying a mixed model to 10 repeated Modified Mini Mental Status Test (3MS) measures over 14 years. Regional gray matter volume (GMV), white matter hyperintensities, and RARs were measured around year 12. RESULTS: Past 3MS decline was related to RAR fragmentation (per SD β = -0.43, 95% confidence interval: -0.73, -0.14) and lower posterior parietal GMV (per standard deviation β = 0.47, 95% confidence interval: 0.14, 0.79). Higher RAR fragmentation was related to lower posterior parietal GMV (Pearson r = -0.39, n = 70, p = 0.0007), which attenuated the association of RAR fragmentation and past cognitive decline by 17%. CONCLUSIONS: Longitudinal studies are warranted to understand the temporal relations and mechanisms linking RAR fragmentation and neurodegeneration.
OBJECTIVES: We examined the extent to which measures of neurodegeneration and cerebrovascular disease explain the rest-activity rhythm (RAR)-cognition link. METHODS: Seventy participants (mean age at MRI = 86, standard deviation (SD) = 2.6; 53% female) had cognitive, MRI, and accelerometer data. The slope of cognitive decline was defined applying a mixed model to 10 repeated Modified Mini Mental Status Test (3MS) measures over 14 years. Regional gray matter volume (GMV), white matter hyperintensities, and RARs were measured around year 12. RESULTS: Past 3MS decline was related to RAR fragmentation (per SD β = -0.43, 95% confidence interval: -0.73, -0.14) and lower posterior parietal GMV (per standard deviation β = 0.47, 95% confidence interval: 0.14, 0.79). Higher RAR fragmentation was related to lower posterior parietal GMV (Pearson r = -0.39, n = 70, p = 0.0007), which attenuated the association of RAR fragmentation and past cognitive decline by 17%. CONCLUSIONS: Longitudinal studies are warranted to understand the temporal relations and mechanisms linking RAR fragmentation and neurodegeneration.
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