Amyloid β concentrations and stable isotope labeling kinetics of human plasma specific to central nervous system amyloidosis
Open accessAbstract
Introduction: Cerebrospinal fluid analysis and other measurements of amyloidosis, such as amyloid‐binding positron emission tomography studies, are limited by cost and availability. There is a need for a more practical amyloid β (Aβ) biomarker for central nervous system amyloid deposition. Methods: We adapted our previously reported stable isotope labeling kinetics protocol to analyze the turnover kinetics and concentrations of Aβ38, Aβ40, and Aβ42 in human plasma. Results: Aβ isoforms have a half‐life of approximately 3 hours in plasma. Aβ38 demonstrated faster turnover kinetics compared with Aβ40 and Aβ42. Faster fractional turnover of Aβ42 relative to Aβ40 and lower Aβ42 and Aβ42/Aβ40 concentrations in amyloid‐positive participants were observed. Discussion: Blood plasma Aβ42 shows similar amyloid‐associated alterations as we have previously reported in cerebrospinal fluid, suggesting a blood‐brain transportation mechanism of Aβ. The stability and sensitivity of plasma Aβ measurements suggest this may be a useful screening test for central nervous system amyloidosis.
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In an 8-year follow-up study of 599 volunteers, cognitively normal PET amyloid-positive people had an elevated risk of developing Alzheimer's disease compared with amyloid-negative people (17·7% vs 8·1%; OR 2·4, 95% CI 1·5-4·0).
“an 8-year follow-up study of 599 volunteers (average age 70 years) in Australia found that cognitively normal PET amyloid-positive people had an elevated risk of developing Alzheimer's disease compared with amyloid negative (17·7% vs 8·1%; OR 2·4, 95% CI 1·5–4·0).184”
From Dementia prevention, intervention, and care: 2020 report of the Lancet Commission (2020) · cites this paper as [184]
The Methods (Participants; page unavailable) describe 41 participants enrolled in the United States, not 599 volunteers in Australia. The Discussion (page unavailable) says longitudinal follow-up is still needed; the paper does not report an eight-year risk comparison or the quoted percentages and odds ratio. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredPlasma Aβ measures now show promise.
“Plasma Aβ measures now show promise [202,203].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [202]
Incorporating biomarkers on a large scale in many settings will require low-cost and minimally invasive biomarkers (e.g., blood or saliva) that are now emerging.
“While imaging/CSF biomarker data on subsets of individuals from well-designed community-based cohorts would provide additional research value, incorporating biomarkers on a large scale in many settings will require low-cost and minimally invasive biomarkers (e.g., blood or saliva) that are now emerging [202–205].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [202]
Over 80% of 266 PET amyloid-positive people did not develop cognitive impairment within 8 years, showing that positive status does not predict impairment for most people in a timeframe that might be a useful prognostic window.
“Over 80% of the 266 people who were PET amyloid-positive did not go onto develop a cognitive impairment within 8 years, showing positive status does not predict impairment for most people in a timeframe that might be a useful prognostic window.”
From Dementia prevention, intervention, and care: 2020 report of the Lancet Commission (2020) · cites this paper as [184]
The Methods (Participants; page unavailable) describe 41 participants, including 18 classified as amyloid-positive, not a cohort of 266 PET-positive people. The Discussion (page unavailable) says longitudinal follow-up would be needed; the copy does not report eight-year cognitive-impairment outcomes or the claimed 80% figure (searched: 266, eight years, longitudinal cognitive impairment). (LLM, conf=0.78)
Experimental — accuracy not yet measuredAt 5-year follow-up, amyloid-positive participants with normal cognition or mild cognitive impairment had the same pattern of increased risk compared with amyloid-negative people (2·6, 1·4-4·9).
“Follow-up at 5 years of amyloid-positive participants with normal cognition or mild cognitive impairment versus amyloid negative people found the same pattern of increased risk (2·6, 1·4–4·9).”
From Dementia prevention, intervention, and care: 2020 report of the Lancet Commission (2020) · cites this paper as [184]
The Methods (Participants; page unavailable) describe amyloid-positive and amyloid-negative groups, but the paper does not report their relative risk at five years. The Discussion (page unavailable) says longitudinal follow-up is still needed. Searches for five-year follow-up and the reported risk estimate found no supporting passage. (LLM, conf=0.78)
Experimental — accuracy not yet measured
Risk of Alzheimer's disease increases per 1 year of age (HR 1·05, 95% CI 0·55-2·0/year) and with APOEε4 status (2·6, 1·4-5·0).
“Risk also increases per 1 year of age (HR 1·05, 95% CI 0·55–2·0/year), and APOEε4 status (2·6, 1·4–5·0).184”
From Dementia prevention, intervention, and care: 2020 report of the Lancet Commission (2020) · cites this paper as [184]
The Methods (Participants; page unavailable) report participants’ ages and APOE genotypes, but not their effects on Alzheimer’s disease risk. Searches for the stated hazard ratios, confidence intervals, and age- or APOE-related risk estimates found no such results in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredFew blood markers exist for the presymptomatic stage of Alzheimer's disease, though some progress has been reported for blood amyloid-β, tau, and NfL.
“Blood biomarkers for the presymptomatic phase of Alzheimer’s disease are largely lacking, although recent progress in the analysis of amyloid-β, tau, and neurofilament light chain (NfL) in the blood have been reported5–10.”
From Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease (2019) · cites this paper as [8]
CNS Aβ deposition can be detected via plasma assessment of Aβ species.
“Recent studies demonstrate the ability to detect CNS Aβ deposition via the use of plasma assessment of Aβ species”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Ovod et al., 2017
Two independent groups demonstrated improved accuracy for plasma Aβ42/Aβ40 using immunoprecipitation-mass spectrometry assays.
“Most recently, 2 independent groups demonstrated improved accuracy for plasma Aβ42/Aβ40 using immunoprecipitation–mass spectrometry assays.19,20”
From Performance of Fully Automated Plasma Assays as Screening Tests for Alzheimer Disease–Related β-Amyloid Status (2019) · cites this paper as [20]
Two recent mass spectrometry-based studies provided overall better accuracies for plasma Aβ42/Aβ40 (AUC, 0.84-0.97 depending on population and reference standard).
“In mass spectrometry–based techniques, 2 recent studies have provided overall better accuracies for plasma Aβ42/Aβ40 (AUC, 0.84-0.97 depending on population and reference standard).19,20”
From Performance of Fully Automated Plasma Assays as Screening Tests for Alzheimer Disease–Related β-Amyloid Status (2019) · cites this paper as [20]
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- Authors
- Ovod, V., Ramsey, K. N., Mawuenyega, K. G., Bollinger, J. G., Hicks, T., Schneider, T., Sullivan, M., Paumier, K., Holtzman, D. M., Morris, J. C., Benzinger, T., Fagan, A. M., Patterson, B. W., & Bateman, R. J.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Bateman, Randall J.
- ORCID
- Venue
- Alzheimer's & Dementia
- Publisher
- Wiley
- Published
- 2017-07-19
- Volume
- 13
- Issue
- 8
- Pages
- 841-849
- ISSN
- 1552-5260 (ISSN-L)
- 1552-5279
- PMC
- PMC5567785
- OpenAlex
- W2736518852
- Cited by
- 585
- References
- 18
- Citations by year
- 2026: 44 · 2025: 44 · 2024: 74 · 2023: 65 · 2022: 84 · 2021: 85 · 2020: 70 · 2019: 66 · 2018: 47 · 2017: 2 · 2015: 1
- FWCI
- 37.40
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Alzheimer s & Dementia (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- MetLife Foundation
- AbbVie
- Amgen
- AstraZeneca
- Biogen
- Eisai
- Pfizer
- Sanofi
- Avid Radiopharmaceuticals
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Amyloidosis: Diagnosis, Treatment, Outcomes
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- amyloid-beta, plasma amyloid-beta
- MeSH terms
- Aged, Amyloidosis, Chromatography, Liquid, Humans, Isotope Labeling, Kinetics, Peptide Fragments, Prospective Studies, ROC Curve, Mass Spectrometry, Biomarkers, Single-Blind Method, Amyloid beta-Peptides, Area Under Curve, Immunoprecipitation
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