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Increased midlife triglycerides predict brain β-amyloid and tau pathology 20 years later

Nägga, Katarina LU ; Gustavsson, Anna-Märta LU ; Stomrud, Erik LU orcid ; Lindqvist, Daniel LU ; van Westen, Danielle LU orcid ; Blennow, Kaj LU ; Zetterberg, Henrik LU ; Melander, Olle LU orcid and Hansson, Oskar LU orcid (2018) In Neurology 90(1). p.1-11
Abstract
Objective To evaluate the effect of midlife lipid levels on Alzheimer brain pathology 20 years later in cognitively normal elderly individuals.
Methods This is a longitudinal cohort study of 318 cognitively normal individuals with data on fasting lipid levels at midlife (mean age 54 years). Presence of β-amyloid (Aβ) and tau pathologies 20 years later (mean age 73 years) were detected by quantifying Alzheimer disease (AD) biomarkers in CSF. In a subset (n = 134), Aβ (18F-flutemetamol) PET was also performed.
Results CSF Aβ42 and Aβ PET revealed Aβ pathology in approximately 20% of the cognitively healthy population and CSF Aβ42/phosphorylated tau (p-tau) ratio indicated both Aβ and tau pathology in 16%. Higher levels of... (More)
Objective To evaluate the effect of midlife lipid levels on Alzheimer brain pathology 20 years later in cognitively normal elderly individuals.
Methods This is a longitudinal cohort study of 318 cognitively normal individuals with data on fasting lipid levels at midlife (mean age 54 years). Presence of β-amyloid (Aβ) and tau pathologies 20 years later (mean age 73 years) were detected by quantifying Alzheimer disease (AD) biomarkers in CSF. In a subset (n = 134), Aβ (18F-flutemetamol) PET was also performed.
Results CSF Aβ42 and Aβ PET revealed Aβ pathology in approximately 20% of the cognitively healthy population and CSF Aβ42/phosphorylated tau (p-tau) ratio indicated both Aβ and tau pathology in 16%. Higher levels of triglycerides in midlife were independently associated with abnormal CSF Aβ42 (odds ratio [OR] 1.34, 95% confidence interval [CI] 1.03–1.75, p = 0.029) and abnormal Aβ42/p-tau ratio (OR 1.46, 95% CI 1.10–1.93; p = 0.009) adjusting for age, sex, APOE ε4, education, and multiple vascular risk factors. Triglycerides were also associated with abnormal Aβ PET in multivariable regression models, but the association was attenuated in the fully adjusted model. Increased levels of medium and large low-density lipoprotein subfractions were significantly associated with abnormal Aβ PET and large high-density lipoprotein particles were associated with decreased risk of abnormal Aβ PET.
Conclusions Increased levels of triglycerides at midlife predict brain Aβ and tau pathology 20 years later in cognitively healthy individuals. Certain lipoprotein subfractions may also be risk factors for Aβ pathology. These findings further support an involvement of lipids in the very early stages of AD development. (Less)
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author
; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Neurology
volume
90
issue
1
pages
1 - 11
publisher
Lippincott Williams & Wilkins
external identifiers
  • scopus:85048603460
  • pmid:29196581
ISSN
1526-632X
DOI
10.1212/WNL.0000000000004749
language
English
LU publication?
yes
id
bb84a79a-0473-4ca1-9458-1d2f3ae3a391
date added to LUP
2019-03-22 11:21:33
date last changed
2024-01-15 14:43:59
@article{bb84a79a-0473-4ca1-9458-1d2f3ae3a391,
  abstract     = {{Objective To evaluate the effect of midlife lipid levels on Alzheimer brain pathology 20 years later in cognitively normal elderly individuals.<br/>Methods This is a longitudinal cohort study of 318 cognitively normal individuals with data on fasting lipid levels at midlife (mean age 54 years). Presence of β-amyloid (Aβ) and tau pathologies 20 years later (mean age 73 years) were detected by quantifying Alzheimer disease (AD) biomarkers in CSF. In a subset (n = 134), Aβ (18F-flutemetamol) PET was also performed.<br/>Results CSF Aβ42 and Aβ PET revealed Aβ pathology in approximately 20% of the cognitively healthy population and CSF Aβ42/phosphorylated tau (p-tau) ratio indicated both Aβ and tau pathology in 16%. Higher levels of triglycerides in midlife were independently associated with abnormal CSF Aβ42 (odds ratio [OR] 1.34, 95% confidence interval [CI] 1.03–1.75, p = 0.029) and abnormal Aβ42/p-tau ratio (OR 1.46, 95% CI 1.10–1.93; p = 0.009) adjusting for age, sex, APOE ε4, education, and multiple vascular risk factors. Triglycerides were also associated with abnormal Aβ PET in multivariable regression models, but the association was attenuated in the fully adjusted model. Increased levels of medium and large low-density lipoprotein subfractions were significantly associated with abnormal Aβ PET and large high-density lipoprotein particles were associated with decreased risk of abnormal Aβ PET.<br/>Conclusions Increased levels of triglycerides at midlife predict brain Aβ and tau pathology 20 years later in cognitively healthy individuals. Certain lipoprotein subfractions may also be risk factors for Aβ pathology. These findings further support an involvement of lipids in the very early stages of AD development.}},
  author       = {{Nägga, Katarina and Gustavsson, Anna-Märta and Stomrud, Erik and Lindqvist, Daniel and van Westen, Danielle and Blennow, Kaj and Zetterberg, Henrik and Melander, Olle and Hansson, Oskar}},
  issn         = {{1526-632X}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{1}},
  pages        = {{1--11}},
  publisher    = {{Lippincott Williams & Wilkins}},
  series       = {{Neurology}},
  title        = {{Increased midlife triglycerides predict brain β-amyloid and tau pathology 20 years later}},
  url          = {{http://dx.doi.org/10.1212/WNL.0000000000004749}},
  doi          = {{10.1212/WNL.0000000000004749}},
  volume       = {{90}},
  year         = {{2018}},
}