Abstract
Plasma phosphatidylcholines (PCs) have been examined in the context of Alzheimer's disease dementia. However, their association with longitudinal changes in amyloid deposition remains unknown. This study investigated the associations of 8 plasma PC levels (PC aa [14:0_14:0], PC aa [16:0_16:0], PC aa [16:0_18:2], PC aa [16:0_22:6], PC aa [18:0_18:0], PC aa [18:0_18:1], PC aa [18:0_20:4], PC aa [18:1_18:1]) with cross-sectional and longitudinal measures of amyloid deposition, Alzheimer's disease–associated neurodegeneration (glucose metabolism and cortical thickness), and cognition (global- and domain-specific) of 1440 cognitively unimpaired participants (47% female, aged 50.7–95.3 years) in the Mayo Clinic Study of Aging. Longitudinally, higher baseline levels of PC aa [16:0_18:2], PC aa [18:0_18:1], and PC aa [18:1_18:1] were associated with slower decline in performance on tests of global cognition and specific cognitive domains. Furthermore, higher baseline levels of plasma PC aa (14:0_14:0) were associated with slower amyloid deposition and cortical thinning after multiple covariable adjustment (age, sex, education, medical comorbidity, dyslipidemia, statin use, and APOE4 allele presence). Our study findings support an independent association between plasma PC aa (14:0_14:0) with slower amyloid deposition and cortical thinning among cognitively unimpaired older adults.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 43-49 |
| Number of pages | 7 |
| Journal | Neurobiology of Aging |
| Volume | 79 |
| DOIs | |
| State | Published - Jul 2019 |
Bibliographical note
Funding Information:This work was supported by the National Institutes of Health , United States/National Institute on Aging grants U01 AG006786 , R01 AG011378 , R01 AG049704 , and RF1 AG55151 , the GHR Foundation and was made possible by the Rochester Epidemiology Project ( R01 AG034676 ). Dr. Li receives research support from the Alzheimer's Association , United States ( NIRG-15-362393 ) and NIH (R21 AG059068 and R01 AG059654). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
Funding Information:
Dr. Li received honoraria and consulting fees from Roche Diagnostics, Abbott Diagnostics, and Diasorin, Inc. and received research support from the National Institutes of Health (NIH), Alzheimer's Association, and Center for Disease Control and Prevention. Dr. Jack consults for Lily and serves on an independent data monitoring board for Roche, but he receives no personal compensation from any commercial entity. He receives research support from NIH and the Alexander Family Alzheimer’s Disease Research Professorship of the Mayo Clinic. Dr. Mielke served as a consultant to Eli Lilly. She receives research support from the National Institutes of Health and unrestricted research grants from Biogen and Lundbeck. Dr. Knopman serves on a Data Safety Monitoring Board for the DIAN study, is an investigator in clinical trials sponsored by Biogen, Lilly Pharmaceuticals and the University of Southern California, and receives research support from the NIH. Dr. Vemuri has no disclosures except funding from the NIH (NIA and NINDS). Mr. Hagen, Miss Fett, and Dr. Bui have nothing to disclose. Dr. Machulda received funding from the NIH. Dr. Ronald Petersen is a consultant for Hoffman-La Roche, Inc, Merck, Inc, Genentech, Inc, and Biogen, Inc and receives honoraria from GE Healthcare and funding from the NIH (Mayo Clinic Alzheimer’s Disease Research Center P50 AG016574 and Mayo Clinic Study of Aging U01 AG006786).
Publisher Copyright:
© 2019 Elsevier Inc.
Keywords
- Amyloid deposition
- Cortical thickness
- Glucose metabolism
- Neurodegeneration
- PC aa (14:0_14:0)
- Phosphatidylcholines
