Cerebrospinal fluid and plasma biomarker trajectories with increasing amyloid deposition in Alzheimer's disease
Open accessAbstract
Failures in Alzheimer's disease (AD) drug trials highlight the need to further explore disease mechanisms and alterations of biomarkers during the development of AD. Using cross-sectional data from 377 participants in the BioFINDER study, we examined seven cerebrospinal fluid (CSF) and six plasma biomarkers in relation to β-amyloid (Aβ) PET uptake to understand their evolution during AD. In CSF, Aβ42 changed first, closely followed by Aβ42/Aβ40, phosphorylated-tau (P-tau), and total-tau (T-tau). CSF neurogranin, YKL-40, and neurofilament light increased after the point of Aβ PET positivity. The findings were replicated using Aβ42, Aβ40, P-tau, and T-tau assays from five different manufacturers. Changes were seen approximately simultaneously for CSF and plasma biomarkers. Overall, plasma biomarkers had smaller dynamic ranges, except for CSF and plasma P-tau which were similar. In conclusion, using state-of-the-art biomarkers, we identified the first changes in Aβ, closely followed by soluble tau. Only after Aβ PET became abnormal, biomarkers of neuroinflammation, synaptic dysfunction, and neurodegeneration were altered. These findings lend in vivo support of the amyloid cascade hypotheses in humans.
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Large cross-sectional neuropathological studies of autopsied brain suggest that tau pathology is prevalent long before amyloid pathology appears, potentially supporting the concept that tau pathology leads to amyloid pathology.
“From large cross-sectional neuropathological studies of autopsied brain 124 , it appears that tau pathology is already prevalent long before amyloid pathology appears, potentially supporting the concept that tau pathology leads to amyloid pathology 125 .”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [124]
Plasma Aβ acts as an endophenotype of AD, simultaneously changing with Aβ status in the brain.
“there is increasing evidence to support that plasma Aβ acts as an endophenotype of AD, which simultaneously changes with Aβ status in the brain.”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [271]
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- Authors
- Palmqvist, S., Insel, P. S., Stomrud, E., Janelidze, S., Zetterberg, H., Brix, B., Eichenlaub, U., Dage, J. L., Chai, X., Blennow, K., Mattsson, N., & Hansson, O.
- Affiliations
- Lund University (SE)
- University of California, San Francisco (US)
- Sahlgrenska University Hospital (SE)
- Euroimmun Medizinische Labordiagnostika (Germany) (DE)
- Eli Lilly (United States) (US)
- Corresponding author
- Palmqvist, Sebastian
- Hansson, Oskar
- ORCID
- Venue
- EMBO Molecular Medicine
- Published
- 2019-11-11
- Volume
- 11
- Issue
- 12
- Pages
- e11170-e11170
- ISSN
- 1757-4676 (ISSN-L)
- 1757-4684
- PMC
- PMC6895602
- OpenAlex
- W2989446795
- Cited by
- 353
- References
- 45
- Citations by year
- 2026: 31 · 2025: 53 · 2024: 48 · 2023: 49 · 2022: 78 · 2021: 55 · 2020: 37 · 2019: 2
- FWCI
- 29.50
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- EMBO Molecular Medicine (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- H2020 European Research Council
- Vetenskapsrådet
- Knut och Alice Wallenbergs Stiftelse
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid deposition, cerebrospinal fluid biomarkers, plasma biomarkers, amyloid PET, amyloid-beta 42, Aβ42/Aβ40 ratio, phosphorylated tau, total tau, neurogranin, YKL-40, neurofilament light chain, amyloid hypothesis, biomarker trajectories, neuroinflammation, synaptic dysfunction, neurodegeneration
- MeSH terms
- Aged, Alzheimer Disease, Female, Humans, Male, Biomarkers, Amyloid beta-Peptides, tau Proteins, Positron-Emission Tomography
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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