Amyloid blood biomarker detects Alzheimer's disease
Open accessAbstract
Alzheimer's disease (AD) is currently incurable, but there is general agreement that a minimally invasive blood biomarker for screening in preclinical stages would be crucial for future therapy. Diagnostic tools for detection of AD are either invasive like cerebrospinal fluid (CSF) biomarkers or expensive such as positron emission tomography (PET) scanning. Here, we determine the secondary structure change of amyloid‐β (Aβ) in human blood. This change used as blood amyloid biomarker indicates prodromal AD and correlates with CSF AD biomarkers and amyloid PET imaging in the cross‐sectional BioFINDER cohort. In a further population‐based longitudinal cohort (ESTHER), the blood biomarker detected AD several years before clinical diagnosis in baseline samples with a positive likelihood ratio of 7.9; that is, those who were diagnosed with AD over the years were 7.9 times more likely to test positive. This assay may open avenues for blood screening of early AD stages as a funnel for further more invasive and expensive tests.
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Aβ began to accumulate up to 15-20 years prior to clinical symptoms of Alzheimer's disease.
“Previous studies revealed that Aβ began to accumulate up to 15–20 years prior to clinical symptoms of Alzheimer’s disease42,43.”
From Integrated algorithm combining plasma biomarkers and cognitive assessments accurately predicts brain β-amyloid pathology (2023) · cites this paper as [42]
The Introduction says Aβ begins to change structure 15–20 years before clinical symptoms and that the altered structures can subsequently aggregate. The Discussion distinguishes this initial misfolding from Aβ burden, so the paper does not establish that Aβ accumulation itself began 15–20 years before symptoms. (LLM, conf=0.83)
Experimental — accuracy not yet measuredBlood biomarkers of amyloid-β misfolding have shown promise in predicting future AD dementia.
“Blood biomarkers of amyloid-β misfolding have shown promise in this regard60,61.”
From Diagnosis of Alzheimer's disease using plasma biomarkers adjusted to clinical probability (2024) · cites this paper as [61]
In plasma samples, the amide I band biomarker was significantly lower for AD individuals using an immuno-infrared-sensor.
“In another study, an immuno‐infrared‐sensor was used for the extraction of the total Aβ fraction from plasma samples, wherein the biomarker amide I band were significantly lower for AD individuals.”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [60]
The test had a positive likelihood ratio of 7.9, indicating good evidence to identify AD in the general population.
“The test had a positive likelihood ratio of 7.9 (ESTHER: Alzheimer’s society in Toronto), which indicated good evidence of this biomarker to identify AD in the general population [60].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [60]
The amide I biomarker could detect AD before clinical diagnosis and without dementia symptoms.
“Amide I biomarker could detect AD before its clinical diagnosis and without dementia symptoms in individuals.”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [60]
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References 39 · Cited by 185
- Authors
- Nabers, A., Perna, L., Lange, J., Mons, U., Schartner, J., Güldenhaupt, J., Saum, K., Janelidze, S., Holleczek, B., Rujescu, D., Hansson, O., Gerwert, K., & Brenner, H.
- Affiliations
- Ruhr University Bochum (DE)
- German Cancer Research Center (DE)
- Lund University (SE)
- Krebsregister Saarland (DE)
- Martin Luther University Halle-Wittenberg (DE)
- Corresponding author
- Gerwert, Klaus
- ORCID
- Venue
- EMBO Molecular Medicine
- Published
- 2018-04-06
- Volume
- 10
- Issue
- 5
- ISSN
- 1757-4676 (ISSN-L)
- 1757-4684
- PMC
- PMC5938617
- OpenAlex
- W2796338238
- Cited by
- 185
- References
- 39
- Citations by year
- 2026: 4 · 2025: 14 · 2024: 20 · 2023: 13 · 2022: 23 · 2021: 33 · 2020: 37 · 2019: 32 · 2018: 9
- FWCI
- 21.84
- 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, cc-by-sa)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- Baden‐Württemberg Ministry of Science, Research and Arts
- German Federal Ministry of Education and Research
- German Federal Ministry of Family, Senior Citizens, Women and Youth
- Saarland Ministry of Social Affairs, Health, Women and Family
- Network Aging Research at the University of Heidelberg
- Protein Research Unit Ruhr within Europe
- Ministry of Innovation, Science and Research of North‐Rhine Westphalia, Germany
- European Research Council, Swedish Research Council
- Swedish Alzheimer Association
- Ministerium für Wissenschaft, Forschung und Kunst Baden‐Württemberg
- Hjärnfonden
- Roche
- GE|GE Healthcare
- Biogen
- Fujirebio Europe
- Eli Lilly and Company
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta, blood biomarkers, secondary structure changes, preclinical Alzheimer's disease, prodromal Alzheimer's disease, cerebrospinal fluid biomarkers, amyloid PET, early diagnosis, likelihood ratios, ESTHER cohort
- MeSH terms
- Aged, Alzheimer Disease, Amyloid, Cross-Sectional Studies, Female, Humans, Male, Middle Aged, ROC Curve, Cohort Studies, Biomarkers, Amyloid beta-Peptides, Protein Structure, Secondary, Positron-Emission Tomography
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