Multimorbidity and neuroimaging biomarkers among cognitively normal persons

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Abstract

Objective: To assess the cross-sectional association between multimorbidity and imaging biomarkers of brain pathology in the population-based Mayo Clinic Study of Aging (MCSA). Methods: The study consisted of 1,449 MCSA participants who were cognitively normal at the time of MRI. A subset of the participants also had 11C-Pittsburgh compound B (n 5 689) and 18fluorodeoxyglucose (n 5 688) PET scans available. Information on multimorbidity (defined as 2 chronic conditions) in the 5 years prior to the first imaging study was captured from the medical record using ICD-9 codes for chronic conditions and the Rochester Epidemiology Project medical records linkage system. The cross-sectional association of multimorbidity and imaging biomarkers was examined using logistic and linear regression models. Results: Among 1,449 cognitively normal participants (mean age 79 years; 50.9% men), 85.4% had multimorbidity (2 chronic conditions). Multimorbidity and severe multimorbidity (4 chronic conditions) were associated with abnormal Alzheimer disease (AD) signature meta-region of interest (meta-ROI) 18F-FDG hypometabolism (odds ratio [OR] 2.03; 95% confidence interval [CI] 1.10-3.77 and OR 2.22; 95% CI 1.18-4.16, respectively), and with abnormal AD signature MRI cortical thickness (OR 1.53; 95% CI 1.09-2.16 and OR 1.76; 95% CI 1.24-2.51, respectively), but was not associated with amyloid accumulation. Conclusions: Multimorbidity was associated with brain pathology through mechanisms independent of amyloid deposition and such neuronal injury and pathology was present before any symptomatic evidence of cognitive impairment. Longitudinal follow-up will provide insights into potential causal associations of multimorbidity with changes in brain pathology.

Original languageEnglish (US)
Pages (from-to)2077-2084
Number of pages8
JournalNeurology
Volume86
Issue number22
DOIs
StatePublished - May 31 2016

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Neuroimaging
Comorbidity
Biomarkers
Odds Ratio
Confidence Intervals
Pathology
International Classification of Diseases
Amyloid
Medical Record Linkage
Linear Models
Alzheimer Disease
Fluorodeoxyglucose F18
Brain
Positron-Emission Tomography
Medical Records
Epidemiology
Logistic Models
Wounds and Injuries
Population

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

@article{7741bb927b864cc792726e7bef80d0e0,
title = "Multimorbidity and neuroimaging biomarkers among cognitively normal persons",
abstract = "Objective: To assess the cross-sectional association between multimorbidity and imaging biomarkers of brain pathology in the population-based Mayo Clinic Study of Aging (MCSA). Methods: The study consisted of 1,449 MCSA participants who were cognitively normal at the time of MRI. A subset of the participants also had 11C-Pittsburgh compound B (n 5 689) and 18fluorodeoxyglucose (n 5 688) PET scans available. Information on multimorbidity (defined as 2 chronic conditions) in the 5 years prior to the first imaging study was captured from the medical record using ICD-9 codes for chronic conditions and the Rochester Epidemiology Project medical records linkage system. The cross-sectional association of multimorbidity and imaging biomarkers was examined using logistic and linear regression models. Results: Among 1,449 cognitively normal participants (mean age 79 years; 50.9{\%} men), 85.4{\%} had multimorbidity (2 chronic conditions). Multimorbidity and severe multimorbidity (4 chronic conditions) were associated with abnormal Alzheimer disease (AD) signature meta-region of interest (meta-ROI) 18F-FDG hypometabolism (odds ratio [OR] 2.03; 95{\%} confidence interval [CI] 1.10-3.77 and OR 2.22; 95{\%} CI 1.18-4.16, respectively), and with abnormal AD signature MRI cortical thickness (OR 1.53; 95{\%} CI 1.09-2.16 and OR 1.76; 95{\%} CI 1.24-2.51, respectively), but was not associated with amyloid accumulation. Conclusions: Multimorbidity was associated with brain pathology through mechanisms independent of amyloid deposition and such neuronal injury and pathology was present before any symptomatic evidence of cognitive impairment. Longitudinal follow-up will provide insights into potential causal associations of multimorbidity with changes in brain pathology.",
author = "Maria Vassilaki and Aakre, {Jeremiah A.} and Mielke, {Michelle M} and Geda, {Yonas Endale} and Kremers, {Walter K} and Alhurani, {Rabe E.} and Machulda, {Mary Margaret} and Knopman, {David S} and Petersen, {Ronald Carl} and Val Lowe and Jack, {Clifford R Jr.} and Roberts, {Rosebud O}",
year = "2016",
month = "5",
day = "31",
doi = "10.1212/WNL.0000000000002624",
language = "English (US)",
volume = "86",
pages = "2077--2084",
journal = "Neurology",
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TY - JOUR

T1 - Multimorbidity and neuroimaging biomarkers among cognitively normal persons

AU - Vassilaki, Maria

AU - Aakre, Jeremiah A.

AU - Mielke, Michelle M

AU - Geda, Yonas Endale

AU - Kremers, Walter K

AU - Alhurani, Rabe E.

AU - Machulda, Mary Margaret

AU - Knopman, David S

AU - Petersen, Ronald Carl

AU - Lowe, Val

AU - Jack, Clifford R Jr.

AU - Roberts, Rosebud O

PY - 2016/5/31

Y1 - 2016/5/31

N2 - Objective: To assess the cross-sectional association between multimorbidity and imaging biomarkers of brain pathology in the population-based Mayo Clinic Study of Aging (MCSA). Methods: The study consisted of 1,449 MCSA participants who were cognitively normal at the time of MRI. A subset of the participants also had 11C-Pittsburgh compound B (n 5 689) and 18fluorodeoxyglucose (n 5 688) PET scans available. Information on multimorbidity (defined as 2 chronic conditions) in the 5 years prior to the first imaging study was captured from the medical record using ICD-9 codes for chronic conditions and the Rochester Epidemiology Project medical records linkage system. The cross-sectional association of multimorbidity and imaging biomarkers was examined using logistic and linear regression models. Results: Among 1,449 cognitively normal participants (mean age 79 years; 50.9% men), 85.4% had multimorbidity (2 chronic conditions). Multimorbidity and severe multimorbidity (4 chronic conditions) were associated with abnormal Alzheimer disease (AD) signature meta-region of interest (meta-ROI) 18F-FDG hypometabolism (odds ratio [OR] 2.03; 95% confidence interval [CI] 1.10-3.77 and OR 2.22; 95% CI 1.18-4.16, respectively), and with abnormal AD signature MRI cortical thickness (OR 1.53; 95% CI 1.09-2.16 and OR 1.76; 95% CI 1.24-2.51, respectively), but was not associated with amyloid accumulation. Conclusions: Multimorbidity was associated with brain pathology through mechanisms independent of amyloid deposition and such neuronal injury and pathology was present before any symptomatic evidence of cognitive impairment. Longitudinal follow-up will provide insights into potential causal associations of multimorbidity with changes in brain pathology.

AB - Objective: To assess the cross-sectional association between multimorbidity and imaging biomarkers of brain pathology in the population-based Mayo Clinic Study of Aging (MCSA). Methods: The study consisted of 1,449 MCSA participants who were cognitively normal at the time of MRI. A subset of the participants also had 11C-Pittsburgh compound B (n 5 689) and 18fluorodeoxyglucose (n 5 688) PET scans available. Information on multimorbidity (defined as 2 chronic conditions) in the 5 years prior to the first imaging study was captured from the medical record using ICD-9 codes for chronic conditions and the Rochester Epidemiology Project medical records linkage system. The cross-sectional association of multimorbidity and imaging biomarkers was examined using logistic and linear regression models. Results: Among 1,449 cognitively normal participants (mean age 79 years; 50.9% men), 85.4% had multimorbidity (2 chronic conditions). Multimorbidity and severe multimorbidity (4 chronic conditions) were associated with abnormal Alzheimer disease (AD) signature meta-region of interest (meta-ROI) 18F-FDG hypometabolism (odds ratio [OR] 2.03; 95% confidence interval [CI] 1.10-3.77 and OR 2.22; 95% CI 1.18-4.16, respectively), and with abnormal AD signature MRI cortical thickness (OR 1.53; 95% CI 1.09-2.16 and OR 1.76; 95% CI 1.24-2.51, respectively), but was not associated with amyloid accumulation. Conclusions: Multimorbidity was associated with brain pathology through mechanisms independent of amyloid deposition and such neuronal injury and pathology was present before any symptomatic evidence of cognitive impairment. Longitudinal follow-up will provide insights into potential causal associations of multimorbidity with changes in brain pathology.

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