Distinct patterns of apolipoprotein C-I, C-II, and C-III isoforms are associated with markers of Alzheimer's disease.

CSF amyloid-β42 apoC-I apoC-II apoC-III apoE apolipoproteins mass spectrometry plasma proteomics

Journal

Journal of lipid research
ISSN: 1539-7262
Titre abrégé: J Lipid Res
Pays: United States
ID NLM: 0376606

Informations de publication

Date de publication:
2021
Historique:
received: 19 05 2020
revised: 09 12 2020
accepted: 11 12 2020
pubmed: 2 2 2021
medline: 11 3 2022
entrez: 1 2 2021
Statut: ppublish

Résumé

Apolipoproteins C-I, C-II, and C-III interact with ApoE to regulate lipoprotein metabolism and contribute to Alzheimer's disease pathophysiology. In plasma, apoC-I and C-II exist as truncated isoforms, while apoC-III exhibits multiple glycoforms. This study aimed to 1) delineate apoC-I, C-II, and C-III isoform profiles in cerebrospinal fluid (CSF) and plasma in a cohort of nondemented older individuals (n = 61), and 2) examine the effect of APOE4 on these isoforms and their correlation with CSF Aβ42, a surrogate of brain amyloid accumulation. The isoforms of the apoCs were immunoaffinity enriched and measured with MALDI-TOF mass spectrometry, revealing a significantly higher percentage of truncated apoC-I and apoC-II in CSF compared with matched plasma, with positive correlation between CSF and plasma. A greater percentage of monosialylated and disialylated apoC-III isoforms was detected in CSF, accompanied by a lower percentage of the two nonsialylated apoC-III isoforms, with significant linear correlations between CSF and plasma. Furthermore, a greater percentage of truncated apoC-I in CSF and apoC-II in plasma and CSF was observed in individuals carrying at least one APOE Ɛ4 allele. Increased apoC-I and apoC-II truncations were associated with lower CSF Aβ42. Finally, monosialylated apoC-III was lower, and disialylated apoC-III greater in the CSF of Ɛ4 carriers. Together, these results reveal distinct patterns of the apoCs isoforms in CSF, implying CSF-specific apoCs processing. These patterns were accentuated in APOE Ɛ4 allele carriers, suggesting an association between APOE4 genotype and Alzheimer's disease pathology with apoCs processing and function in the brain.

Identifiants

pubmed: 33518512
pii: S0022-2275(20)43718-6
doi: 10.1194/jlr.RA120000919
pmc: PMC7859854
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

100014

Subventions

Organisme : NIA NIH HHS
ID : P50 AG005142
Pays : United States
Organisme : NIA NIH HHS
ID : R43 AG069552
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG067063
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG054434
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG055770
Pays : United States
Organisme : NIA NIH HHS
ID : R21 AG056518
Pays : United States

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article.

Auteurs

Yueming Hu (Y)

Isoformix Inc, Phoenix, Arizona, USA.

Cristiana Meuret (C)

University of Southern California, Los Angeles, California, USA.

Ashley Martinez (A)

University of Southern California, Los Angeles, California, USA.

Hussein N Yassine (HN)

University of Southern California, Los Angeles, California, USA. Electronic address: hyassine@usc.edu.

Dobrin Nedelkov (D)

Isoformix Inc, Phoenix, Arizona, USA. Electronic address: dobrin.nedelkov@isoformix.com.

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Classifications MeSH