Performance of plasma Aβ42/40, measured using a fully automated immunoassay, across a broad patient population in identifying amyloid status.
Alzheimer’s disease
Amyloid positron emission tomography
Amyloid β
Centiloid
Plasma Aβ42/40
Journal
Alzheimer's research & therapy
ISSN: 1758-9193
Titre abrégé: Alzheimers Res Ther
Pays: England
ID NLM: 101511643
Informations de publication
Date de publication:
04 09 2023
04 09 2023
Historique:
received:
17
06
2023
accepted:
24
08
2023
medline:
6
9
2023
pubmed:
5
9
2023
entrez:
4
9
2023
Statut:
epublish
Résumé
Plasma biomarkers have emerged as promising screening tools for Alzheimer's disease (AD) because of their potential to detect amyloid β (Aβ) accumulation in the brain. One such candidate is the plasma Aβ42/40 ratio (Aβ42/40). Unlike previous research that used traditional immunoassay, recent studies that measured plasma Aβ42/40 using fully automated platforms reported promising results. However, its utility should be confirmed using a broader patient population, focusing on the potential for early detection. We recruited 174 participants, including healthy controls (HC) and patients with clinical diagnoses of AD, frontotemporal lobar degeneration, dementia with Lewy bodies/Parkinson's disease, mild cognitive impairment (MCI), and others, from a university memory clinic. We examined the performance of plasma Aβ42/40, measured using the fully automated high-sensitivity chemiluminescence enzyme (HISCL) immunoassay, in detecting amyloid-positron emission tomography (PET)-derived Aβ pathology. We also compared its performance with that of Simoa-based plasma phosphorylated tau at residue 181 (p-tau181), glial fibrillary acidic protein (GFAP), and neurofilament light (NfL). Using the best cut-off derived from the Youden Index, plasma Aβ42/40 yielded an area under the receiver operating characteristic curve (AUC) of 0.949 in distinguishing visually assessed Plasma Aβ42/40 measured using the fully automated HISCL platform showed excellent performance in identifying Aβ accumulation in the brain in a well-characterized cohort. This equipment may be useful for screening amyloid pathology because it has the potential to detect early amyloid pathology and is readily applied in clinical settings.
Sections du résumé
BACKGROUND
Plasma biomarkers have emerged as promising screening tools for Alzheimer's disease (AD) because of their potential to detect amyloid β (Aβ) accumulation in the brain. One such candidate is the plasma Aβ42/40 ratio (Aβ42/40). Unlike previous research that used traditional immunoassay, recent studies that measured plasma Aβ42/40 using fully automated platforms reported promising results. However, its utility should be confirmed using a broader patient population, focusing on the potential for early detection.
METHODS
We recruited 174 participants, including healthy controls (HC) and patients with clinical diagnoses of AD, frontotemporal lobar degeneration, dementia with Lewy bodies/Parkinson's disease, mild cognitive impairment (MCI), and others, from a university memory clinic. We examined the performance of plasma Aβ42/40, measured using the fully automated high-sensitivity chemiluminescence enzyme (HISCL) immunoassay, in detecting amyloid-positron emission tomography (PET)-derived Aβ pathology. We also compared its performance with that of Simoa-based plasma phosphorylated tau at residue 181 (p-tau181), glial fibrillary acidic protein (GFAP), and neurofilament light (NfL).
RESULTS
Using the best cut-off derived from the Youden Index, plasma Aβ42/40 yielded an area under the receiver operating characteristic curve (AUC) of 0.949 in distinguishing visually assessed
CONCLUSION
Plasma Aβ42/40 measured using the fully automated HISCL platform showed excellent performance in identifying Aβ accumulation in the brain in a well-characterized cohort. This equipment may be useful for screening amyloid pathology because it has the potential to detect early amyloid pathology and is readily applied in clinical settings.
Identifiants
pubmed: 37667408
doi: 10.1186/s13195-023-01296-5
pii: 10.1186/s13195-023-01296-5
pmc: PMC10476307
doi:
Substances chimiques
amyloid beta-protein (1-42)
0
Amyloid beta-Peptides
0
Amyloidogenic Proteins
0
Banques de données
UMIN-CTR
['UMIN000032027']
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
149Informations de copyright
© 2023. BioMed Central Ltd., part of Springer Nature.
Références
Lancet Neurol. 2016 Jun;15(7):673-684
pubmed: 27068280
Brain. 2011 Sep;134(Pt 9):2456-77
pubmed: 21810890
Alzheimers Dement. 2011 May;7(3):270-9
pubmed: 21514249
Alzheimers Dement. 2023 Apr;19(4):1393-1402
pubmed: 36150024
Am J Psychiatry. 1984 Nov;141(11):1356-64
pubmed: 6496779
Brain Behav. 2022 Mar;12(3):e2499
pubmed: 35134278
Nat Rev Neurosci. 2020 Jan;21(1):21-35
pubmed: 31780819
Alzheimers Res Ther. 2022 Dec 27;14(1):195
pubmed: 36575454
Nat Med. 2022 Dec;28(12):2555-2562
pubmed: 36456833
Sci Rep. 2020 Sep 11;10(1):14950
pubmed: 32917930
Alzheimers Dement. 2015 Aug;11(8):964-74
pubmed: 25824567
Neurology. 2019 Oct 22;93(17):e1647-e1659
pubmed: 31371569
Mov Disord. 2017 Jun;32(6):853-864
pubmed: 28467028
Alzheimers Dement. 2018 Apr;14(4):535-562
pubmed: 29653606
JAMA Neurol. 2021 Nov 1;78(11):1375-1382
pubmed: 34542571
J Psychiatr Res. 1975 Nov;12(3):189-98
pubmed: 1202204
Clin Transl Imaging. 2015;3(1):13-26
pubmed: 25741488
Neurology. 2023 Jan 17;100(3):e264-e274
pubmed: 36175151
Alzheimers Dement. 2015 Jan;11(1):1-15.e1-4
pubmed: 25443857
Neural Regen Res. 2014 Jan 1;9(1):69-75
pubmed: 25206745
Psychopharmacol Bull. 1988;24(4):637-9
pubmed: 3249765
Brain. 2021 Dec 16;144(11):3505-3516
pubmed: 34259835
Nat Med. 2022 Sep;28(9):1797-1801
pubmed: 35953717
Alzheimers Res Ther. 2021 Mar 27;13(1):67
pubmed: 33773598
J Neuropathol Exp Neurol. 2012 Apr;71(4):266-73
pubmed: 22437338
Lancet Neurol. 2022 Jan;21(1):66-77
pubmed: 34838239
Alzheimers Dement. 2023 Apr;19(4):1117-1134
pubmed: 36574591
Neurology. 2013 Jan 29;80(5):496-503
pubmed: 23359374
JAMA Neurol. 2021 Dec 1;78(12):1471-1483
pubmed: 34661615
Nat Med. 2020 Mar;26(3):387-397
pubmed: 32123386
Alzheimers Dement. 2023 Apr;19(4):1204-1215
pubmed: 35950735
Neurology. 2011 Mar 15;76(11):1006-14
pubmed: 21325651
Alzheimers Res Ther. 2019 Mar 21;11(1):27
pubmed: 30902090
Lancet Neurol. 2020 May;19(5):422-433
pubmed: 32333900
Biochem Biophys Res Commun. 2021 Oct 22;576:22-26
pubmed: 34478915
J Alzheimers Dis. 2009;16(2):277-85
pubmed: 19221417
Alzheimers Dement. 2011 May;7(3):263-9
pubmed: 21514250
Biometrics. 1988 Sep;44(3):837-45
pubmed: 3203132
Alzheimers Res Ther. 2022 Jun 23;14(1):86
pubmed: 35739591