Association of serum Apolipoprotein B with cerebrospinal fluid biomarkers of Alzheimer's pathology.


Journal

Annals of clinical and translational neurology
ISSN: 2328-9503
Titre abrégé: Ann Clin Transl Neurol
Pays: United States
ID NLM: 101623278

Informations de publication

Date de publication:
10 2020
Historique:
received: 01 05 2020
revised: 23 06 2020
accepted: 16 07 2020
pubmed: 11 9 2020
medline: 18 8 2021
entrez: 10 9 2020
Statut: ppublish

Résumé

To examine whether apolipoprotein B (ApoB), apolipoprotein A-1 (ApoA1), or their ratio (ApoB/A1) were associated with early changes in cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD) pathology in elderly adults with subjective cognitive decline (SCD). This study included 507 objective cognitive normal participants from the Chinese Alzheimer's Biomarker and LifestylE (CABLE) database including 288 cognitive normal participants (CN) and 219 SCD. Multiple linear regression models were used to examine the associations of apolipoproteins with CSF AD biomarkers. Compared with control group, SCD participants with significant AD biological characteristics had lower ApoB levels (P = 0.0461). In total participants, lower level of serum ApoB was associated with decreases in CSF Aβ42 (P = 0.0015) and Aβ42/40 (P = 0.0081) as well as increases in CSF p-tau/Aβ42 (P < 0.0001) and t-tau/Aβ42 (P = 0.0013), independent of APOEɛ4 status. In further subgroup analysis, these associations were more significant in SCD participants (ApoB × Diagnose: P < 0.05). In addition, lower levels of ApoB were also found associated with increases in p-tau in the SCD subgroup (P = 0.0263). Furthermore, these protective associations were more significant in the overweight participants (ApoB × weight: P < 0.05). Results showed no association between ApoA1 and CSF biomarkers. This study is the first to find protective associations of serum ApoB with CSF AD core biomarkers, especially in SCD individuals. It indicated that ApoB may be a potential biomarker for preclinical AD and may play different roles in different stages of AD.

Identifiants

pubmed: 32910550
doi: 10.1002/acn3.51153
pmc: PMC7545610
doi:

Substances chimiques

Amyloid beta-Peptides 0
Apolipoproteins B 0
Biomarkers 0
Peptide Fragments 0
tau Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1766-1778

Informations de copyright

© 2020 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.

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Auteurs

Hao Hu (H)

Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.

Lan Tan (L)

Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.

Yan-Lin Bi (YL)

Department of Anesthesiology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.

Wei Xu (W)

Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.

Lin Tan (L)

Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.

Xue-Ning Shen (XN)

Department of Neurology and Institute of Neurology, WHO Collaborating Center for Research and Training in Neurosciences, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.

Xiao-He Hou (XH)

Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.

Ya-Hui Ma (YH)

Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.

Qiang Dong (Q)

Department of Neurology and Institute of Neurology, WHO Collaborating Center for Research and Training in Neurosciences, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.

Jin-Tai Yu (JT)

Department of Neurology and Institute of Neurology, WHO Collaborating Center for Research and Training in Neurosciences, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.

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Classifications MeSH