Association of serum Apolipoprotein B with cerebrospinal fluid biomarkers of Alzheimer's pathology.
Aged
Alzheimer Disease
/ blood
Amyloid beta-Peptides
/ cerebrospinal fluid
Apolipoproteins B
/ blood
Biomarkers
/ cerebrospinal fluid
Cognition
/ physiology
Cognitive Dysfunction
/ blood
Data Management
Female
Humans
Male
Neuropsychological Tests
Peptide Fragments
/ cerebrospinal fluid
tau Proteins
/ cerebrospinal fluid
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
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
1766-1778Informations de copyright
© 2020 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.
Références
Alzheimers Res Ther. 2019 Jul 31;11(1):66
pubmed: 31366409
Acta Neuropathol. 2018 Dec;136(6):821-853
pubmed: 30488277
Ann Neurol. 2010 Jan;67(1):122-31
pubmed: 20186853
J Alzheimers Dis. 2013;35(4):751-60
pubmed: 23481685
Neurosci Lett. 1992 Jan 6;134(2):264-6
pubmed: 1375354
Alzheimers Dement. 2017 Mar;13(3):296-311
pubmed: 27825022
Sci Am. 1984 Nov;251(5):58-66
pubmed: 6390676
Arch Gen Psychiatry. 2010 Apr;67(4):414-22
pubmed: 20368517
Alzheimers Dement. 2018 Apr;14(4):535-562
pubmed: 29653606
J Alzheimers Dis. 2017;56(2):687-697
pubmed: 28035918
JAMA. 2012 Jun 20;307(23):2499-506
pubmed: 22797450
Dement Geriatr Cogn Disord. 2007;24(3):177-84
pubmed: 17641528
Alzheimers Dement. 2014 Nov;10(6):844-52
pubmed: 24798886
Lancet Neurol. 2016 Jun;15(7):673-684
pubmed: 27068280
J Clin Endocrinol Metab. 2019 Jul 1;104(7):2942-2952
pubmed: 30802284
Eur J Neurol. 2018 Jan;25(1):59-70
pubmed: 28872215
Neurobiol Aging. 2010 Aug;31(8):1275-83
pubmed: 20472326
EMBO Mol Med. 2016 Jun 01;8(6):595-608
pubmed: 27025652
Proc Natl Acad Sci U S A. 2009 Apr 21;106(16):6820-5
pubmed: 19346482
Neurobiol Aging. 2000 Jan-Feb;21(1):27-30
pubmed: 10794845
Arch Neurol. 2012 Feb;69(2):223-9
pubmed: 22332189
JAMA Neurol. 2019 Jul 1;76(7):809-817
pubmed: 31135820
Alzheimers Dement. 2010 May;6(3):202-11.e7
pubmed: 20451868
J Alzheimers Dis. 2014;38(1):201-9
pubmed: 23948937
Biochem Biophys Res Commun. 1998 Nov 27;252(3):711-5
pubmed: 9837771
Alzheimers Dement. 2010 Jan;6(1):11-24
pubmed: 20129317
J Neuropathol Exp Neurol. 1998 Dec;57(12):1168-74
pubmed: 9862640
Sci Transl Med. 2013 Jun 12;5(189):189ra77
pubmed: 23761040
Neurosci Lett. 2006 Nov 6;408(1):68-72
pubmed: 16997467
Neurology. 2009 May 19;72(20):1741-6
pubmed: 19451529
Alzheimers Dement. 2013 Sep;9(5):481-7
pubmed: 23232269
Neurology. 2006 Jun 27;66(12):1837-44
pubmed: 16801647
J Alzheimers Dis. 2016 Mar 29;52(2):561-72
pubmed: 27031486
Age (Dordr). 2016 Dec;38(5-6):465-473
pubmed: 27663235
Neurobiol Aging. 2006 Mar;27(3):471-81
pubmed: 16213630
J Neuropathol Exp Neurol. 2003 Nov;62(11):1087-95
pubmed: 14656067
Alzheimers Res Ther. 2019 Jan 17;11(1):8
pubmed: 30654834
JAMA Neurol. 2016 Jun 1;73(6):698-705
pubmed: 27064267
Alzheimers Dement. 2011 May;7(3):280-92
pubmed: 21514248