Cited by 724Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchAir Quality and Health Impacts

Improved discrimination of AD patients using β-amyloid (1-42) and tau levels in CSF

Open access
Hulstaert, F., Blennow, K., Ivanoiu, A., Schoonderwaldt, H.C., Riemenschneider, M., Deyn, P.P. De, Bancher, C., Cras, P. +6 more·1999·Neurology

Abstract

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1212/wnl.52.8.1555

Cites

75 of 75 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Neurofibrillary tangles are made of hyperphosphorylated tau protein.

    “These deposits are composed of hyperphosphorylated tau-protein (Hulstaert et al., 1999).”

    From Dynamics of Gray Matter Loss in Alzheimer's Disease (2003) · cites this paper as Hulstaert et al., 1999

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 31

  1. Van de Voorde A, Vanmechelen E, Vandermeeren M, Dessaint F, Beeckman W, Cras P. Detection of tau in cerebrospinal fluid. In: Iqbal K, Mortimer JA, Winblad B, Wisniewski HM, eds. Research advances in Alzheimer's disease and related disorders. Chichester: John Wiley & Sons Ltd., 1995:189 -195.
  2. Vanderstichele H, Van Gool S, Brock P, et al. Monitoring of chemotherapy-induced neurotoxicity in children using CSF markers, a longitudinal study. Neurobiol Aging 1998;19:S168. Abstract.
  3. Hesse C, Minthon L, Wallin A, et al. Tau protein and ␤-amyloid (1-42) in cerebrospinal fluid from Alzheimer's disease patients and controls. Neurobiol Aging 1998;19:S163. Abstract. References
  4. Kanheman D. Attention and effort. Englewood Cliffs, NJ: Prentice Hall, 1973.
  5. Brayne C, Calloway P. Normal ageing, impaired cognitive function and senile dementia of Alzheimer type: a continuum? Lancet 1988;1:1265-1267.
  6. Fillit HM. The clinical significance of normal cognitive decline in late life. In: Fillit HM, Butler RN. Cognitive decline. Strat- egies for prevention. Oxford: Oxford University Press, 1997: 1-7.
  7. Launer LJ, Masaki K, Petrovich H, Foley D, Havlik RJ. The association between midlife blood pressure levels and late-life cognitive function. JAMA 1995;274:1846 -1851.
  8. White LR, Foley DJ, Havlik RJ. Lifestyle risk factors for cog- nitive impairment. In: Fillit HM, Butler RN. Cognitive de- cline. Strategies for prevention. Oxford: Oxford University Press, 1997:23-32.
  9. Amaducci L, Baldereschi M, Di Carlo A, et al. Prevalence of chronic diseases in older Italians: comparing self-reported and clinical diagnoses. Int J Epidemiol 1997;26:995-1002.
  10. McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of the Department of Health and Human Services Task Force on Alzheimer's disease. Neurology 1984;34:939 -944.
  11. World Health Organization. International statistical classifi- cation of diseases and related health problems, 10th revision (ICD-10). Chapter V, categories F00 -F99. Mental, behav- ioural, and developmental disorders, clinical description and diagnostic guidelines. Geneva: World Health Organization, 1992.
  12. Folstein MF, Folstein SE, McHugh PR. "Mini-Mental State": a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975;12:189 -198.
  13. Barigazzi R, Della Sala S, Laiacona M, Spinnler H, Valenti V. Esplorazione testistica della memoria di prosa. Ric Psicol 1987;1:50 -80.
  14. Lawton MP, Brody EM. Assessment of older people: self main- taining and instrumental activities of daily living. Gerontolo- gist 1969;9:179 -186.
  15. Leoci CL, Centonze S, Guerra V, Cisternino AM, Misciagna G. Validazione e riproducibilita `di un questionario di frequenza alimentare semi-quantitativo autosomministrato. Giorn Ital Nutr Clin Prev 1993;1:58 -59.
  16. La Rue A, Koehler KM, Wayne SJ, Chiulli SJ, Haaland KY, Garry PJ. Nutritional status and cognitive functioning in a normally aging sample: a 6-year reassessment. Am J Clin Nutr 1997;65:20 -29.
  17. Manna C, Galletti P, Cucciolla V, Moltedo O, Leone A, Zappia V. The protective effect of the olive oil polyphenol (3,3- dihydroxyphenyl)-ethanol counteract reactive oxygen meta- bolite-indeced cytotoxicity in Caco-2 cells. J Nutr 1997;127: 286 -292.
  18. Kalmijn S, Feskens EJ, Launer LJ, Kromhout D. Polyunsatu- rated fatty acids, antioxidants, and cognitive functions in very old men. Am J Epidemiol 1997;145:33-41. References
  19. Santo Pietro MJ, Rigrodsdy S. Patterns of oral-verbal perse- verations. Brain Lang 1984;23:148 -158.
  20. Shindler AG, Caplan LR, Hier DB. Intrusions and persevera- tions. Brain Lang 1984;23:148 -158.
  21. Hudson AJ. Perseveration. Brain 1968;91:571-582.
  22. Helmick JW, Berg CB. Perseverations in brain injured adults. J Commun Disord 1976;9:143-156.
  23. Sandson J, Albert ML. Perseveration in behavioral neurology. Neurology 1987;37:1736 -1741.
  24. Na DL, Adair JC, Williamson DJG, Schwartz RL, Haws B, Heilman KM. Dissociation of sensory-attentional from motor- intentional neglect. J Neurol Neurosurg Psychiatry 1998;64: 331-338.
  25. Samuelsson H, Hjelmquist E, Naver H, Blomstrand C. Visuo- spatial neglect and an ipsilesional bias during the start of performance on conventional tests of neglect. Clinical Neuro- psychologist 1996;10:15-24.
  26. Posner MI, Walker JA, Friedrich FJ, Rafal RD. Effects of parietal injury on covert orienting of attention. J Neurosci 1984;4:1863-1874.
  27. Heilman KM, Valenstein E. Mechanisms underlying hemispa- tial neglect. Ann Neurol 1979;5:166 -170.
  28. Kinsbourne M. A model for the mechanism of unilateral ne- glect in space. Trans Am Neurol Assoc 1970;95:143-146.
  29. Kinsbourne M. Hemi-neglect and hemispheric rivalry. In: Weinstein EA, Friedland RP, eds. Hemi-inattention and hemi- sphere specialization. New York: Raven Press, 1977:41-49.
  30. Goldberg E, Costa L. Qualitative indices in neuropsychologi- cal assessment: executive deficit following prefrontal lesions. In: Adams K, Grant I, eds. Neuropsychological assessment of neuropsychiatric disorders. London & New York: Oxford Uni- versity Press, 1985:48 -64.
  31. Denny-Brown D, Chambers RA. The parietal lobe and behav- ior. Res Publ Assoc Res Nerv Ment Dis 1958;36:35-117.

Cited by

Sorted by citations

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)
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
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

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 ›

Are you an author, or do you see a problem with this page? Request a review