Improved discrimination of AD patients using β-amyloid (1-42) and tau levels in CSF
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Background and Aims: Epidemiology studies have shown that cardiovascular (CV) disease is primarily responsible for the mortality associated with increased pulmonary environmental particle (PM10) exposure. The mechanisms involved in PM10 mediated CV effects are unknown although changes in plasma viscosity and in the homoeostasis of blood coagulation have been implicated. It was hypothesised that PM10 exposure would result in an inflammatory response and enhance the activation of the extrinsic coagulation mechanisms in pulmonary and vascular cells in culture. Methods: Primary human monocyte derived macrophages and human umbilical cord vein endothelial, human alveolar type II epithelial (A549), and human bronchial epithelial (16HBE) cells were tested for their inflammatory and procoagulant response to PM10 exposure. IL-8, tissue factor (TF), and tissue plasminogen activator (tPA) gene expression and protein release, and coagulation enhancing ability of culture media were determined 6 and 24 hours following exposure. Results: The culture media from macrophages and 16HBE bronchial epithelial cells, but not A549 cells, exposed to PM10 had an enhanced ability to cause clotting. Furthermore, H2O2 also increased the clotting activity. Apoptosis was significantly increased in macrophages exposed to PM10 and LPS as shown by annexin V binding. TF gene expression was enhanced in macrophages exposed to PM10, and HUVEC tissue factor and tPA gene and protein expression were inhibited. Conclusions: These data indicate that PM10 has the ability to alter macrophage, epithelial, and endothelial cell function to favour blood coagulation via activation of the extrinsic pathway and inhibition of fibrinolysis pathways.
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Neurofibrillary tangles are made of hyperphosphorylated tau protein.
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CSF markers for incipient Alzheimer's disease
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Self-citationDynamics of Gray Matter Loss in Alzheimer's Disease
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Self-citationPlasma and Cerebrospinal Fluid Levels of Amyloid β Proteins 1-40 and 1-42 in Alzheimer Disease
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Self-citationEvaluation of CSF-tau and CSF-Aβ42 as diagnostic markers for Alzheimer disease in clinical practice
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Self-citationAmnestic MCI or prodromal Alzheimer's disease?
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Current state of Alzheimer’s fluid biomarkers
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Self-citationDiagnosis-Independent Alzheimer Disease Biomarker Signature in Cognitively Normal Elderly People
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Total and phosphorylated tau protein as biological markers of Alzheimer’s disease
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Self-citationStandardization of measurement of β-amyloid<sub>(1-42)</sub>in cerebrospinal fluid and plasma
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Proteome profiling in cerebrospinal fluid reveals novel biomarkers of Alzheimer's disease
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Self-citationMicroRNA Profiling of CSF Reveals Potential Biomarkers to Detect Alzheimer`s Disease
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Altered Proteins in the Aging Brain
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Combined CSF tau, p-tau181 and amyloid-β 38/40/42 for diagnosing Alzheimer’s disease
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Self-citationCSF biomarkers for mild cognitive impairment
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Self-citationPreclinical AD predicts decline in memory and executive functions in subjective complaints
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<i>APOE</i> ε4 allele is associated with reduced cerebrospinal fluid levels of Aβ42
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T1rho MRI and CSF biomarkers in diagnosis of Alzheimer's disease
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NT1-Tau Is Increased in CSF and Plasma of CJD Patients, and Correlates with Disease Progression
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- Authors
- Hulstaert, F., Blennow, K., Ivanoiu, A., Schoonderwaldt, H. C., Riemenschneider, M., Deyn, P. P. D., Bancher, C., Cras, P., Wiltfang, J., Mehta, P. D., Iqbal, K., Pottel, H., Vanmechelen, E., & Vanderstichele, H.
- Affiliations
- Cliniques Universitaires Saint-Luc (BE)
- ORCID
- Venue
- Neurology
- Published
- 1999-05
- Volume
- 52
- Issue
- 8
- Pages
- 1555-1555
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2035680108
- Cited by
- 724
- References
- 75
- Citations by year
- 2026: 1 · 2025: 8 · 2024: 22 · 2023: 11 · 2022: 14 · 2021: 26 · 2020: 20 · 2019: 13 · 2018: 17 · 2017: 24 · 2016: 23 · 2015: 27 · 2014: 38 · 2013: 33 · 2012: 33
- FWCI
- 17.74
- Type
- journal article
- Language
- en
- Open access
- green
- lirias.kuleuven.be
- Licence
- other-oa
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Lirias (KU Leuven) (submittedVersion, other-oa)
- Digital Access to Libraries (submittedVersion)
- GRO (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- U.S. Department of Veterans Affairs
- European Commission
- Samsung Biomedical Research Institute
- Samsung
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Keywords
- Alzheimer's disease, amyloid-beta 42, tau protein, cerebrospinal fluid biomarkers, differential diagnosis
- MeSH terms
- Adult, Aged, Aged, 80 and over, Alzheimer Disease, Humans, Middle Aged, Quality Control, Amyloid beta-Peptides, tau Proteins
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