TY - JOUR
T1 - Longitudinal association between phosphatidylcholines, neuroimaging measures of Alzheimer's disease pathophysiology, and cognition in the Mayo Clinic Study of Aging
AU - Li, Danni
AU - Hagen, Clinton
AU - Fett, Ashely R.
AU - Bui, Hai H.
AU - Knopman, David
AU - Vemuri, Prashanthi
AU - Machulda, Mary M.
AU - Jack, Clifford R.
AU - Petersen, Ronald C.
AU - Mielke, Michelle M.
N1 - 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.
Publisher Copyright:
© 2019 Elsevier Inc.
PY - 2019/7
Y1 - 2019/7
N2 - 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.
AB - 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.
KW - Amyloid deposition
KW - Cortical thickness
KW - Glucose metabolism
KW - Neurodegeneration
KW - PC aa (14:0_14:0)
KW - Phosphatidylcholines
UR - http://www.scopus.com/inward/record.url?scp=85064557098&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85064557098&partnerID=8YFLogxK
U2 - 10.1016/j.neurobiolaging.2019.03.005
DO - 10.1016/j.neurobiolaging.2019.03.005
M3 - Article
C2 - 31026621
AN - SCOPUS:85064557098
VL - 79
SP - 43
EP - 49
JO - Neurobiology of Aging
JF - Neurobiology of Aging
SN - 0197-4580
ER -