Title
Association of CD14 with incident dementia and markers of brain aging and injury
Date Issued
21 January 2020
Access level
open access
Resource Type
journal article
Author(s)
Pase M.P.
Himali J.J.
Beiser A.S.
DeCarli C.
McGrath E.R.
Satizabal C.L.
Aparicio H.J.
Adams H.H.H.
Reiner A.P.
Longstreth W.T.
Fornage M.
Tracy R.P.
Lopez O.
Psaty B.M.
Levy D.
Seshadri S.
Bis J.C.
Publisher(s)
Lippincott Williams and Wilkins
Abstract
OBJECTIVE: To test the hypothesis that the inflammatory marker plasma soluble CD14 (sCD14) associates with incident dementia and related endophenotypes in 2 community-based cohorts. METHODS: Our samples included the prospective community-based Framingham Heart Study (FHS) and Cardiovascular Health Study (CHS) cohorts. Plasma sCD14 was measured at baseline and related to the incidence of dementia, domains of cognitive function, and MRI-defined brain volumes. Follow-up for dementia occurred over a mean of 10 years (SD 4) in the FHS and a mean of 6 years (SD 3) in the CHS. RESULTS: We studied 1,588 participants from the FHS (mean age 69 ± 6 years, 47% male, 131 incident events) and 3,129 participants from the CHS (mean age 72 ± 5 years, 41% male, 724 incident events) for the risk of incident dementia. Meta-analysis across the 2 cohorts showed that each SD unit increase in sCD14 was associated with a 12% increase in the risk of incident dementia (95% confidence interval 1.03-1.23; p = 0.01) following adjustments for age, sex, APOE ε4 status, and vascular risk factors. Higher levels of sCD14 were associated with various cognitive and MRI markers of accelerated brain aging in both cohorts and with a greater progression of brain atrophy and a decline in executive function in the FHS. CONCLUSION: sCD14 is an inflammatory marker related to brain atrophy, cognitive decline, and incident dementia.
Start page
e254
End page
e266
Volume
94
Issue
3
Language
English
OCDE Knowledge area
Neurociencias
Neurología clínica
Scopus EID
2-s2.0-85078393222
PubMed ID
Source
Neurology
ISSN of the container
00283878
Sponsor(s)
M.P.P. is funded by a National Heart Foundation of Australia Future Leader Fellowship (102,052). The Framingham Heart Study is supported by the National Heart, Lung, and Blood Institute (contract no. N01-HC-25195 and no. HHSN268201500001I) and by grants from the National Institute on Aging (R01 AG054076, R01 AG049607, R01 AG058589, R01 AG059421, U01 AG049505, U01 AG052409) and the National Institute of Neurologic Disorders and Stroke (NS017950 and UH2 NS100605 as part of MarkVCID). H.J.A. is supported by a National Institute on Aging Research Supplement to Promote Diversity in Health-Related Research (R01AG054076-02S1) and through support from Boston University School of Medicine's Jack Spivack Neuroscience scholarship and Aram V. Chobanian Assistant Professorship. C.D. directs the UC Davis Alzheimer's Disease Center with funding from the NIH (P30 AG010182). CHS research was supported by contracts HHSN268201200036C, HHSN268200800007C, HHSN268201800001C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086, and N01HC15103, and grants U01HL080295 and U01HL130114 from the National Heart, Lung, and Blood Institute, with additional contribution from the National Institute of Neurologic Disorders and Stroke. Additional support was provided by R01AG023629, R01AG15928, and R01AG20098 from the National Institute on Aging. A full list of principal CHS investigators and institutions can be found at CHS-NHLBI.org .
Sources of information:
Directorio de Producción Científica
Scopus