Longitudinal association between phosphatidylcholines, neuroimaging measures of Alzheimer's disease pathophysiology, and cognition in the Mayo Clinic Study of Aging

Research output: Contribution to journalArticle

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 languageEnglish (US)
Pages (from-to)43-49
Number of pages7
JournalNeurobiology of aging
Volume79
DOIs
StatePublished - Jul 1 2019

Fingerprint

Phosphatidylcholines
Neuroimaging
Cognition
Alzheimer Disease
Amyloid
Social Adjustment
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Sex Education
Dyslipidemias
Comorbidity

Keywords

  • Amyloid deposition
  • Cortical thickness
  • Glucose metabolism
  • Neurodegeneration
  • PC aa (14:0_14:0)
  • Phosphatidylcholines

ASJC Scopus subject areas

  • Neuroscience(all)
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology

Cite this

@article{90317e221b76468c8eef5bff6fd40cd9,
title = "Longitudinal association between phosphatidylcholines, neuroimaging measures of Alzheimer's disease pathophysiology, and cognition in the Mayo Clinic Study of Aging",
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.",
keywords = "Amyloid deposition, Cortical thickness, Glucose metabolism, Neurodegeneration, PC aa (14:0_14:0), Phosphatidylcholines",
author = "Danni Li and Clinton Hagen and Fett, {Ashely R.} and Bui, {Hai H.} and Knopman, {David S} and Vemuri, {Prashanthi D} and Machulda, {Mary Margaret} and Jack, {Clifford R Jr.} and Petersen, {Ronald Carl} and Mielke, {Michelle M}",
year = "2019",
month = "7",
day = "1",
doi = "10.1016/j.neurobiolaging.2019.03.005",
language = "English (US)",
volume = "79",
pages = "43--49",
journal = "Neurobiology of Aging",
issn = "0197-4580",
publisher = "Elsevier Inc.",

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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 S

AU - Vemuri, Prashanthi D

AU - Machulda, Mary Margaret

AU - Jack, Clifford R Jr.

AU - Petersen, Ronald Carl

AU - Mielke, Michelle M

PY - 2019/7/1

Y1 - 2019/7/1

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

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U2 - 10.1016/j.neurobiolaging.2019.03.005

DO - 10.1016/j.neurobiolaging.2019.03.005

M3 - Article

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SP - 43

EP - 49

JO - Neurobiology of Aging

JF - Neurobiology of Aging

SN - 0197-4580

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