Altered bile acid profile in mild cognitive impairment and Alzheimer's disease: Relationship to neuroimaging and CSF biomarkers.
Aged
Alzheimer Disease
/ cerebrospinal fluid
Amyloid beta-Peptides
/ cerebrospinal fluid
Bile Acids and Salts
/ blood
Biomarkers
/ cerebrospinal fluid
Cognitive Dysfunction
/ cerebrospinal fluid
Female
Fluorodeoxyglucose F18
/ metabolism
Humans
Magnetic Resonance Imaging
Male
Neuroimaging
Positron-Emission Tomography
Prospective Studies
tau Proteins
/ cerebrospinal fluid
Alzheimer's disease
Amyloid-β
Bile acid
Brain glucose metabolism
CSF biomarkers
Gut-liver-brain axis
MRI
Metabolomics
PET
Journal
Alzheimer's & dementia : the journal of the Alzheimer's Association
ISSN: 1552-5279
Titre abrégé: Alzheimers Dement
Pays: United States
ID NLM: 101231978
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
20
03
2018
revised:
03
08
2018
accepted:
21
08
2018
pubmed:
20
10
2018
medline:
11
4
2020
entrez:
20
10
2018
Statut:
ppublish
Résumé
Bile acids (BAs) are the end products of cholesterol metabolism produced by human and gut microbiome co-metabolism. Recent evidence suggests gut microbiota influence pathological features of Alzheimer's disease (AD) including neuroinflammation and amyloid-β deposition. Serum levels of 20 primary and secondary BA metabolites from the AD Neuroimaging Initiative (n = 1562) were measured using targeted metabolomic profiling. We assessed the association of BAs with the "A/T/N" (amyloid, tau, and neurodegeneration) biomarkers for AD: cerebrospinal fluid (CSF) biomarkers, atrophy (magnetic resonance imaging), and brain glucose metabolism ([ Of 23 BAs and relevant calculated ratios after quality control procedures, three BA signatures were associated with CSF Aβ This is the first study to show serum-based BA metabolites are associated with "A/T/N" AD biomarkers, providing further support for a role of BA pathways in AD pathophysiology. Prospective clinical observations and validation in model systems are needed to assess causality and specific mechanisms underlying this association.
Identifiants
pubmed: 30337152
pii: S1552-5260(18)33521-0
doi: 10.1016/j.jalz.2018.08.012
pmc: PMC6454538
mid: NIHMS994005
pii:
doi:
Substances chimiques
Amyloid beta-Peptides
0
Bile Acids and Salts
0
Biomarkers
0
tau Proteins
0
Fluorodeoxyglucose F18
0Z5B2CJX4D
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
232-244Subventions
Organisme : NIA NIH HHS
ID : R01 AG019771
Pays : United States
Organisme : NLM NIH HHS
ID : R00 LM011384
Pays : United States
Organisme : NLM NIH HHS
ID : K99 LM011384
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG024904
Pays : United States
Organisme : NINDS NIH HHS
ID : P50 NS053488
Pays : United States
Organisme : NLM NIH HHS
ID : R01 LM011360
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG010161
Pays : United States
Organisme : NIA NIH HHS
ID : RF1 AG051550
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG015819
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG046171
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG046152
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG010124
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG010133
Pays : United States
Organisme : NIA NIH HHS
ID : R03 AG054936
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG017917
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH098260
Pays : United States
Organisme : NIBIB NIH HHS
ID : R01 EB022574
Pays : United States
Organisme : NIA NIH HHS
ID : U19 AG024904
Pays : United States
Organisme : NIA NIH HHS
ID : K01 AG049050
Pays : United States
Organisme : NLM NIH HHS
ID : R01 LM012535
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG061359
Pays : United States
Informations de copyright
Copyright © 2018. Published by Elsevier Inc.
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