Amyloid-β Oligomers Relate to Cognitive Decline in Alzheimer's Disease
Open accessAbstract
BACKGROUND: Amyloid-β (Aβ)-oligomers are neurotoxic isoforms of Aβ and are a potential diagnostic biomarker for Alzheimer's disease (AD). OBJECTIVES: 1) Analyze the potential of Aβ-oligomer concentrations in cerebrospinal fluid (CSF) to diagnose and predict progression to AD in a large clinical study sample. 2) Monitor Aβ-oligomer concentrations over-time, both in early and advanced stages of AD. 3) Examine the relation between Aβ-oligomer levels in CSF and cognitive functioning. METHODS: 24 non-demented, 61 mild cognitive impairment (MCI), and 64 AD patients who underwent lumbar puncture and cognitive testing at baseline and follow-up were selected from the memory clinic based Amsterdam Dementia Cohort. CSF samples were analyzed for standard AD-biomarkers and Aβ-oligomer levels using a validated in-house Aβ-oligomer specific enzyme-linked immunosorbent assay. Aβ-oligomer levels were analyzed as indicators of disease progression (follow-up AD diagnosis) and cognitive decline, respectively. RESULTS: Patient groups did not differ in Aβ-oligomer concentrations at baseline or follow-up. Baseline CSF Aβ-oligomer levels were similar in MCI patients that develop AD as in stable MCI patients. MCI and AD patients showed an annual decrease in Aβ-oligomer levels of 9.4% and 6.8%, respectively. A decrease in Aβ-oligomer levels over time was strongly associated with more severe cognitive decline in AD patients. CONCLUSION: Despite the limited diagnostic potential of Aβ-oligomer levels in CSF to differentiate between patient groups, and between MCI-AD and MCI-stable patients, changes in CSF Aβ-oligomer levels were related to cognitive decline. Therefore, CSF Aβ-oligomers may aid in the selection of patients with a more aggressive disease course.
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Extracellular amyloid-β deposits like senile plaques might represent a relatively innocuous endpoint of the amyloid-β aggregation process, while soluble and smaller amyloid-β aggregates show higher toxicity and a greater correlation with cognitive decline and neurodegeneration.
“Extracellular Aβ deposits like senile plaques might represent a relatively innocuous endpoint of the Aβ aggregation process, while soluble and smaller Aβ aggregates show higher toxicity and a greater correlation with cognitive decline and neurodegeneration [58, 76].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [58]
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- Authors
- Jongbloed, W., Bruggink, K. A., Kester, M. I., Visser, P.-J., Scheltens, P., Blankenstein, M. A., Verbeek, M. M., Teunissen, C. E., & Veerhuis, R.
- Affiliations
- Amsterdam Neuroscience (NL)
- Radboud University Medical Center (NL)
- Maastricht University (NL)
- Corresponding author
- Veerhuis, Robert
- ORCID
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2015-03-03
- Volume
- 45
- Issue
- 1
- Pages
- 35-43
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W1502002613
- Cited by
- 68
- References
- 37
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 16 · 2022: 6 · 2021: 6 · 2020: 3 · 2019: 8 · 2018: 5 · 2017: 6 · 2016: 5 · 2015: 4
- FWCI
- 5.43
- Type
- journal article
- Language
- en
- Open access
- green
- pure.amsterdamumc.nl
- Licence
- other-oa
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- Research Publications (Maastricht University) (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Pure Amsterdam UMC (submittedVersion, other-oa)
- Radboud Repository (Radboud University) (submittedVersion)
- VU Research Portal (submittedVersion)
- Research Publications (Maastricht University) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- European Commission (37670)
- Maastricht Universitair Medisch Centrum
- Leids Universitair Medisch Centrum
- Center for Translational Molecular Medicine (02N-101)
- Radboud Universitair Medisch Centrum
- Stichting Dioraphte
- 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
- amyloid-beta oligomers, Alzheimer's disease
- MeSH terms
- Aged, Alzheimer Disease, Cognition Disorders, Enzyme-Linked Immunosorbent Assay, Female, Follow-Up Studies, Humans, Male, Mental Status Schedule, Middle Aged, Peptide Fragments, Statistics as Topic, Amyloid beta-Peptides
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