Michelle R Caunca1,2,3, Karen Siedlecki4, Ying Kuen Cheung5, Noam Alperin2,6, Sang H Lee2,6, Mitchell S V Elkind7,8, Ralph L Sacco1,2,3, Clinton B Wright9, Tatjana Rundek1,2,3. 1. Department of Public Health Sciences, Miller School of Medicine, University of Miami, Miami, Florida. 2. Evelyn F. McKnight Brain Institute, University of Miami, Miami, Florida. 3. Department of Neurology, Miller School of Medicine, University of Miami, Miami, Florida. 4. Department of Psychology, Fordham University, New York, New York. 5. Department of Biostatistics, Mailman School of Public Health, Columbia University, New York, New York. 6. Department of Radiology, Miller School of Medicine, University of Miami, Miami, Florida. 7. Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York. 8. Department of Neurology, Valegos College of Physicians and Surgeons, Columbia University, New York, New York. 9. National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, Maryland.
Abstract
BACKGROUND: How cerebrovascular disease and neurodegeneration affect each other to impact cognition is not yet known. We aimed to test whether Alzheimer's disease-signature (AD) cortical thickness mediates the association between cholinergic white matter lesion load and change in domain-specific cognition. METHODS: Clinically stroke-free participants from the Northern Manhattan Study with both regional white matter hyperintensity volume (WMHV) and gray matter measurements were included (N = 894). Tract-specific WMHVs were quantified through FSL using the Johns Hopkins University white matter tract atlas. We used Freesurfer 5.1 to estimate regional cortical thickness. We fit structural equation models, including multiple indicator latent change score models, to examine associations between white matter hyperintensity volume (WMHV) in cholinergic tracts, AD-signature region cortical thickness (CT), and domain-specific cognition. RESULTS: Our sample (N = 894) had a mean (SD) age = 70 (9) years, years of education = 10 (5), 63% women, and 67% Hispanics/Latinos. Greater cholinergic WMHV was significantly related to worse processing speed at baseline (standardized β = -0.17, SE = 0.05, p = .001) and over time (standardized β = -0.28, SE = 0.09, p = .003), with a significant indirect effect of AD-signature region CT (baseline: standardized β = -0.02, SE = 0.01, p = .023; change: standardized β = -0.03, SE = 0.02, p = .040). CONCLUSIONS: Cholinergic tract WMHV is associated with worse processing speed, both directly and indirectly through its effect on AD-signature region CT.
BACKGROUND: How cerebrovascular disease and neurodegeneration affect each other to impact cognition is not yet known. We aimed to test whether Alzheimer's disease-signature (AD) cortical thickness mediates the association between cholinergic white matter lesion load and change in domain-specific cognition. METHODS: Clinically stroke-free participants from the Northern Manhattan Study with both regional white matter hyperintensity volume (WMHV) and gray matter measurements were included (N = 894). Tract-specific WMHVs were quantified through FSL using the Johns Hopkins University white matter tract atlas. We used Freesurfer 5.1 to estimate regional cortical thickness. We fit structural equation models, including multiple indicator latent change score models, to examine associations between white matter hyperintensity volume (WMHV) in cholinergic tracts, AD-signature region cortical thickness (CT), and domain-specific cognition. RESULTS: Our sample (N = 894) had a mean (SD) age = 70 (9) years, years of education = 10 (5), 63% women, and 67% Hispanics/Latinos. Greater cholinergic WMHV was significantly related to worse processing speed at baseline (standardized β = -0.17, SE = 0.05, p = .001) and over time (standardized β = -0.28, SE = 0.09, p = .003), with a significant indirect effect of AD-signature region CT (baseline: standardized β = -0.02, SE = 0.01, p = .023; change: standardized β = -0.03, SE = 0.02, p = .040). CONCLUSIONS: Cholinergic tract WMHV is associated with worse processing speed, both directly and indirectly through its effect on AD-signature region CT.
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