Plasma Aβ42/40 ratio, p-tau181, GFAP, and NfL across the Alzheimer's disease continuum: A cross-sectional and longitudinal study in the AIBL cohort.
Alzheimer's disease
amyloid beta
blood biomarkers
brain amyloid beta
diagnosis
glial fibrillary acidic protein
longitudinal monitoring
neurofilament light
p-tau181
single molecule array
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:
04 2023
04 2023
Historique:
revised:
22
05
2022
received:
08
02
2022
accepted:
23
05
2022
medline:
17
4
2023
pubmed:
28
12
2022
entrez:
27
12
2022
Statut:
ppublish
Résumé
Plasma amyloid beta (Aβ)1-42/Aβ1-40 ratio, phosphorylated-tau181 (p-tau181), glial fibrillary acidic protein (GFAP), and neurofilament light (NfL) are putative blood biomarkers for Alzheimer's disease (AD). However, head-to-head cross-sectional and longitudinal comparisons of the aforementioned biomarkers across the AD continuum are lacking. Plasma Aβ1-42, Aβ1-40, p-tau181, GFAP, and NfL were measured utilizing the Single Molecule Array (Simoa) platform and compared cross-sectionally across the AD continuum, wherein Aβ-PET (positron emission tomography)-negative cognitively unimpaired (CU Aβ-, n = 81) and mild cognitive impairment (MCI Aβ-, n = 26) participants were compared with Aβ-PET-positive participants across the AD continuum (CU Aβ+, n = 39; MCI Aβ+, n = 33; AD Aβ+, n = 46) from the Australian Imaging, Biomarker & Lifestyle Flagship Study of Ageing (AIBL) cohort. Longitudinal plasma biomarker changes were also assessed in MCI (n = 27) and AD (n = 29) participants compared with CU (n = 120) participants. In addition, associations between baseline plasma biomarker levels and prospective cognitive decline and Aβ-PET load were assessed over a 7 to 10-year duration. Lower plasma Aβ1-42/Aβ1-40 ratio and elevated p-tau181 and GFAP were observed in CU Aβ+, MCI Aβ+, and AD Aβ+, whereas elevated plasma NfL was observed in MCI Aβ+ and AD Aβ+, compared with CU Aβ- and MCI Aβ-. Among the aforementioned plasma biomarkers, for models with and without AD risk factors (age, sex, and apolipoprotein E (APOE) ε4 carrier status), p-tau181 performed equivalent to or better than other biomarkers in predicting a brain Aβ-/+ status across the AD continuum. However, for models with and without the AD risk factors, a biomarker panel of Aβ1-42/Aβ1-40, p-tau181, and GFAP performed equivalent to or better than any of the biomarkers alone in predicting brain Aβ-/+ status across the AD continuum. Longitudinally, plasma Aβ1-42/Aβ1-40, p-tau181, and GFAP were altered in MCI compared with CU, and plasma GFAP and NfL were altered in AD compared with CU. In addition, lower plasma Aβ1-42/Aβ1-40 and higher p-tau181, GFAP, and NfL were associated with prospective cognitive decline and lower plasma Aβ1-42/Aβ1-40, and higher p-tau181 and GFAP were associated with increased Aβ-PET load prospectively. These findings suggest that plasma biomarkers are altered cross-sectionally and longitudinally, along the AD continuum, and are prospectively associated with cognitive decline and brain Aβ-PET load. In addition, although p-tau181 performed equivalent to or better than other biomarkers in predicting an Aβ-/+ status across the AD continuum, a panel of biomarkers may have superior Aβ-/+ status predictive capability across the AD continuum. Area under the curve (AUC) of p-tau181 ≥ AUC of Aβ42/40, GFAP, NfL in predicting PET Aβ-/+ status (Aβ-/+). AUC of Aβ42/40+p-tau181+GFAP panel ≥ AUC of Aβ42/40/p-tau181/GFAP/NfL for Aβ-/+. Longitudinally, Aβ42/40, p-tau181, and GFAP were altered in MCI versus CU. Longitudinally, GFAP and NfL were altered in AD versus CU. Aβ42/40, p-tau181, GFAP, and NfL are associated with prospective cognitive decline. Aβ42/40, p-tau181, and GFAP are associated with increased PET Aβ load prospectively.
Substances chimiques
amyloid beta-protein (1-42)
0
Amyloid beta-Peptides
0
Glial Fibrillary Acidic Protein
0
Apolipoprotein E4
0
Biomarkers
0
tau Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1117-1134Informations de copyright
© 2022 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.
Références
Villemagne VL, Burnham S, Bourgeat P, et al. Amyloid beta deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer's disease: a prospective cohort study. Lancet Neurol. 2013;12:357-367.
Bateman RJ, Xiong C, Benzinger TL, et al. Clinical and biomarker changes in dominantly inherited Alzheimer's disease. N Engl J Med. 2012;367:795-804.
Simren J, Leuzy A, Karikari TK, et al. The diagnostic and prognostic capabilities of plasma biomarkers in Alzheimer's disease. Alzheimers Dement. 2021;17:1145-1156.
Schindler SE, Bateman RJ. Combining blood-based biomarkers to predict risk for Alzheimer's disease dementia. Nature Aging. 2021;1:26-28.
Verberk IMW, Thijssen E, Koelewijn J, et al. Combination of plasma amyloid beta(1-42/1-40) and glial fibrillary acidic protein strongly associates with cerebral amyloid pathology. Alzheimers Res Ther. 2020;12:118.
Karikari TK, Pascoal TA, Ashton NJ, et al. Blood phosphorylated tau 181 as a biomarker for Alzheimer's disease: a diagnostic performance and prediction modelling study using data from four prospective cohorts. Lancet Neurol. 2020;19:422-433.
Elahi FM, Casaletto KB, Joie RL, et al. Plasma biomarkers of astrocytic and neuronal dysfunction in early- and late-onset Alzheimer's disease. Alzheimers Dement. 2020;16:681-95.
Ashton NJ, Pascoal TA, Karikari TK, et al. Plasma p-tau231: a new biomarker for incipient Alzheimer's disease pathology. Acta Neuropathol. 2021;14:709-724.
Karikari TK, Benedet AL, Ashton NJ, et al. Diagnostic performance and prediction of clinical progression of plasma haracte-tau181 in the Alzheimer's Disease Neuroimaging Initiative. Mol Psychiatry. 2021;26:429-442.
Chatterjee P, Elmi M, Goozee K, et al. Ultrasensitive detection of plasma amyloid-beta as a biomarker for cognitively normal elderly individuals at risk of Alzheimer's disease. J Alzheimers Dis. 2019;71:775-783.
Verberk IMW, Slot RE, Verfaillie SCJ, et al. Plasma amyloid as prescreener for the earliest haracter pathological changes. Ann Neurol. 2018;84:648-658.
Chatterjee P, Pedrini S, Stoops E, et al. Plasma glial fibrillary acidic protein is elevated in cognitively normal older adults at risk of Alzheimer's disease. Transl Psychiatry. 2021;11:27.
Janelidze S, Stomrud E, Palmqvist S, et al. Plasma beta-amyloid in Alzheimer's disease and vascular disease. Sci Rep. 2016;6:26801.
Nakamura A, Kaneko N, Villemagne VL, et al. High performance plasma amyloid-beta biomarkers for Alzheimer's disease. Nature. 2018;554:249-254.
Janelidze S, Mattsson N, Palmqvist S, et al. Plasma P-tau181 in Alzheimer's disease: relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer's dementia. Nat Med. 2020;26:379-386.
Chatterjee P, Pedrini S, Ashton NJ, et al. Diagnostic and prognostic plasma biomarkers for preclinical Alzheimer's disease. Alzheimers Dement. 2022;18:1141-1154.
Benedet AL, Mila-Aloma M, Vrillon A, et al. Differences between plasma and cerebrospinal fluid glial fibrillary acidic protein levels across the Alzheimer disease continuum. JAMA Neurol. 2021;78:1471-1483.
Weston PSJ, Poole T, Ryan NS, et al. Serum neurofilament light in familial Alzheimer disease: a marker of early neurodegeneration. Neurology. 2017;89:2167-2175.
Preische O, Schultz SA, Apel A, et al. Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer's disease. Nat Med. 2019;25:277-283.
Quiroz YT, Zetterberg H, Reiman EM, et al. Plasma neurofilament light chain in the presenilin 1 E280A autosomal dominant Alzheimer's disease kindred: a cross-sectional and longitudinal cohort study. Lancet Neurol. 2020;19:513-521.
Ellis KA, Bush AI, Darby D, et al. The Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging: methodology and baseline characteristics of 1112 individuals recruited for a longitudinal study of Alzheimer's disease. Int Psychogeriatr. 2009;21:672-687.
McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology. 1984;34:939-944.
Petersen RC, Smith GE, Waring SC, Ivnik RJ, Tangalos EG, Kokmen E. Mild cognitive impairment: clinical characterization and outcome. Arch Neurol. 1999;56:303-308.
Winblad B, Palmer K, Kivipelto M, et al. Mild cognitive impairment-beyond controversies, towards a consensus: report of the International Working Group on Mild Cognitive Impairment. J Intern Med. 2004;256:240-246.
Bourgeat P, Dore V, Fripp J, et al. Implementing the centiloid transformation for (11)C-PiB and beta-amyloid (18)F-PET tracers using CapAIBL. Neuroimage. 2018;183:387-393.
Folstein MF, Folstein SE, McHugh PR. “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12:189-198.
Morris JC. The Clinical Dementia Rating (CDR): current version and scoring rules. Neurology. 1993;43:2412-2414.
Donohue MC, Sperling RA, Salmon DP, et al. The preclinical Alzheimer cognitive composite: measuring amyloid-related decline. JAMA Neurol. 2014;71:961-970.
Xiao Z, Wu X, Wu W, et al. Plasma biomarker profiles and the correlation with cognitive function across the clinical spectrum of Alzheimer's disease. Alzheimers Res Ther. 2021;13:123.
Suarez-Calvet M, Karikari TK, Ashton NJ, et al. Novel tau biomarkers phosphorylated at T181, T217 or T231 rise in the initial stages of the preclinical Alzheimer's continuum when only subtle changes in Abeta pathology are detected. EMBO Mol Med. 2020;12:e12921.
Pereira JB, Janelidze S, Smith R, et al. Plasma GFAP is an early marker of amyloid-beta but not tau pathology in Alzheimer's disease. Brain. 2021;144:3505-3516.
Chatterjee P, Goozee K, Sohrabi HR, et al. Association of plasma neurofilament light chain with neocortical amyloid-beta load and cognitive performance in cognitively normal elderly participants. J Alzheimers Dis. 2018;63:479-487.
Mattsson N, Andreasson U, Zetterberg H, Blennow K, Alzheimer's disease neuroimaging I. Association of plasma neurofilament light with neurodegeneration in patients with Alzheimer disease. JAMA Neurol. 2017;74:557-566.
Ashton NJ, Janelidze S, Al Khleifat A, et al. A multicentre validation study of the diagnostic value of plasma neurofilament light. Nat Commun. 2021;12:3400.
Benkert P, Meier S, Schaedelin S, et al. Serum neurofilament light chain for individual prognostication of disease activity in people with multiple sclerosis: a retrospective modelling and validation study. Lancet Neurol. 2022;21:246-257.
Pilotto A, Imarisio A, Conforti F, et al. Plasma NfL, clinical subtypes and motor progression in Parkinson's disease. Parkinsonism Relat Disord. 2021;87:41-47.
Huang Y, Huang C, Zhang Q, Shen T, Sun J. Serum NFL discriminates Parkinson disease from essential tremor and reflect motor and cognition severity. BMC Neurol. 2022;22:39.
Weinhofer I, Rommer P, Zierfuss B, et al. Neurofilament light chain as a potential biomarker for monitoring neurodegeneration in X-linked adrenoleukodystrophy. Nat Commun. 2021;12:1816.
Beach TG, Monsell SE, Phillips LE, Kukull W. Accuracy of the clinical diagnosis of Alzheimer disease at National Institute on Aging Alzheimer Disease Centers, 2005-2010. J Neuropathol Exp Neurol. 2012;71:266-273.
Clark CM, Pontecorvo MJ, Beach TG, et al. Cerebral PET with florbetapir compared with neuropathology at autopsy for detection of neuritic amyloid-beta plaques: a prospective cohort study. Lancet Neurol. 2012;11:669-678.
Palmqvist S, Zetterberg H, Blennow K, et al. Accuracy of brain amyloid detection in clinical practice using cerebrospinal fluid beta-amyloid 42: a cross-validation study against amyloid positron emission tomography. JAMA Neurol. 2014;71:1282-1289.
Janelidze S, Teunissen CE, Zetterberg H, et al. Head-to-head comparison of 8 plasma amyloid-beta 42/40 assays in Alzheimer disease. JAMA Neurol. 2021;78:1375-1382.
Cicognola C, Janelidze S, Hertze J, et al. Plasma glial fibrillary acidic protein detects Alzheimer pathology and predicts future conversion to Alzheimer dementia in patients with mild cognitive impairment. Alzheimers Res Ther. 2021;13:68.
O'Connor A, Karikari TK, Poole T, et al. Plasma haracte-tau181 in presymptomatic and symptomatic familial Alzheimer's disease: a longitudinal cohort study. Mol Psychiatry. 2020;26:5967-5976.
Rodriguez JL, Karikari TK, Suarez-Calvet M, et al. Plasma p-tau181 accurately predicts Alzheimer's disease pathology at least 8 years prior to post-mortem and improves the clinical haracterization of cognitive decline. Acta Neuropathol. 2020;140:267-278.
Seppala TT, Herukka SK, Hanninen T, et al. Plasma Abeta42 and Abeta40 as markers of cognitive change in follow-up: a prospective, longitudinal, population-based cohort study. J Neurol Neurosurg Psychiatry. 2010;81:1123-1127.
Giudici KV, de SoutoBarreto P, Guyonnet S, et al. Assessment of plasma amyloid-beta42/40 and cognitive decline among community-dwelling older adults. JAMA Netw Open. 2020;3:e2028634.
Moscoso A, Grothe MJ, Ashton NJ, et al. Longitudinal associations of blood phosphorylated tau181 and neurofilament light chain with neurodegeneration in Alzheimer disease. JAMA Neurol. 2021;78:396-406.
Thijssen EH, La Joie R, Wolf A, et al. Diagnostic value of plasma phosphorylated tau181 in Alzheimer's disease and frontotemporal lobar degeneration. Nat Med. 2020;26:387-397.
Mielke MM, Syrjanen JA, Blennow K, et al. Plasma and CSF neurofilament light: relation to longitudinal neuroimaging and cognitive measures. Neurology. 2019;93:e252-e260.
Schindler SE, Bollinger JG, Ovod V, et al. High-precision plasma beta-amyloid 42/40 predicts current and future brain amyloidosis. Neurology. 2019;93:e1647-e1659.
Shen XN, Huang YY, Chen SD, et al. Plasma phosphorylated-tau181 as a predictive biomarker for Alzheimer's amyloid, tau and FDG PET status. Transl Psychiatry. 2021;11:585.