Hostname: page-component-7479d7b7d-8zxtt Total loading time: 0 Render date: 2024-07-11T01:17:55.291Z Has data issue: false hasContentIssue false
  • English
  • Français

Reduced beta-amyloid sensitivity for platelet–monocyte aggregates in EDTA blood of alzheimer patients

Published online by Cambridge University Press:  17 August 2017

Michaela Defrancesco ,
Josef Marksteiner  and
Christian Humpel
Michaela Defrancesco
Affiliation:
Department of Psychiatry and Psychosomatics, Division of Psychiatry I, Medical University of Innsbruck, Innsbruck, Austria
Josef Marksteiner
Affiliation:
Department of Psychiatry and Psychotherapy A, General Hospital, Hall, Austria
Christian Humpel*
Affiliation:
Laboratory of Psychiatry and Experimental Alzheimer's Research, Medical University of Innsbruck, Innsbruck, Austria
*
Correspondence should be addressed: Christian Humpel, PhD, Department of Psychiatry, Psychotherapy and Psychosomatics, Anichstr. 35, A-6020 Innsbruck, Austria. Phone: +43-512-504-23712; Fax: +43-512-504-23713. E-mail: christian.humpel@i-med.ac.at.
Get access Rights & Permissions [Opens in a new window]

Abstract

Alzheimer´s disease (AD) is a severe neurodegenerative brain disorder characterized by beta-amyloid plaques, Tau pathology, inflammation, neurodegeneration, and cerebrovascular dysfunction. Besides that, alterations in monocytes and platelets have been reported in the blood of Alzheimer patients. In the present study, we measured circulating levels of platelet–monocyte aggregates in EDTA blood of cognitively healthy participants and 40 AD patients, and examined their changes induced by stimulation with beta-amyloid peptides. We measured CD14, CD62P, and CD42a using fluorescence-activated cell scanning (FACS) analysis. Our data show that the levels of circulating monocyte–platelet aggregates were not different between healthy controls and AD patients. However, incubation with beta-amyloid-40, −42, and pyroglutamate-beta-amyloid increased the platelet–monocyte aggregation in healthy subjects, but not AD patients. Our data conclude that the interaction between monocytes and platelets is not altered in whole blood of AD patients, but their sensitivity toward beta-amyloid peptides is decreased. There might be a critical link between the interaction of platelets and monocytes in AD, which has to be explored in further studies.

Keywords

Alzheimer´s diseasebloodbiomarkers
Type
Brief Report
Information
International Psychogeriatrics , Volume 30 , Issue 1 , January 2018 , pp. 147 - 152
Copyright
Copyright © International Psychogeriatric Association 2017 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Bush, A.I. et al. (1990). The amyloid precursor protein of Alzheimer's disease is released by human platelets. The Journal of Biological Chemistry, 265, 15977–15983.Google Scholar
Chen, M., Inestrosa, N. C., Ross, G. S. and Fernandez, H. L. (1995). Platelets are the primary source of amyloid beta-peptide in human blood. Biochemical and Biophysical Research Communications, 213, 96–103.CrossRefGoogle ScholarPubMed
de la Torre, J. C. and Mussivand, T. (1993). Can disturbed brain microcirculation cause Alzheimer's disease? Neurological Research, 15, 146–153.Google Scholar
Fernandez, H. L. (1995). Platelets are the primary source of amyloid beta-peptide in human blood. Biochemical and Biophysical Research Communications, 213, 96–103.Google Scholar
Giri, R. et al. (2000). Beta-amyloid-induced migration of monocytes across human brain endothelial cells involves RAGE and PECAM-1. American Journal of Physiology. Cell Physiology, 279, 1772–81.Google Scholar
Järemo, P., Milovanovic, M., Buller, C., Nilsson, S. and Winblad, B. (2013). P-selectin paradox and dementia of the Alzheimer type: circulating P-selectin is increased but platelet-bound P-selectin after agonist provocation is compromised. Scandinavian Journal of Clinical and Laboratory Investigation, 73, 170–174. doi: 10.3109/00365513.2013.764572. Epub 2013 Feb 19.Google Scholar
Jung, B. K., Cho, C. H., Moon, K. C., Sung Hur, D., Yoon, J.-A. and Yoon, S.-Y. (2014). Detection of platelet-monocyte aggregates by the ADAM® image cytometer. International Journal of Medical Sciences, 11, 1228–1233. http://doi.org/10.7150/ijms.10008 Google Scholar
Liu, Y. et al. (2005). LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide. Brain, 128, 1778–1789.Google Scholar
Lucin, K. M. and Wyss-Coray, T. (2009). Immune activation in brain aging and neurodegeneration: too much or too little?. Neuron, 64, 110–122.Google Scholar
Marksteiner, J., Imarhiagbe, D., Defrancesco, M., Deisenhammer, E. A., Kemmler, G. and Humpel, C. (2013). Analysis of 27 vascular-related proteins reveals that NT-proBNP is a potential biomarker for Alzheimer's disease and mild cognitive impairment: a pilot-study. Experimental Gerontology, 50, 114–121. doi: 10.1016/j.exger.2013.12.001. Epub 2013 Dec 10.Google Scholar
Pickford, F. et al. (2008). The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice. The Journal of Clinical Investigation, 118, 2190–2199.Google Scholar
Reed-Geaghan, E. G., Reed, Q. W., Cramer, P. E. and Landreth, G. E. (2010). Deletion of CD14 attenuates AD pathology by influencing the brain's inflammatory milieu. The Journal of Neuroscience : The Official Journal of the Society for Neuroscience, 30, 15369–15373. doi: 10.1523/JNEUROSCI.2637-10.2010.CrossRefGoogle ScholarPubMed
Roher, A. E. et al. (2009). Amyloid beta peptides in human plasma and tissues and their significance for Alzheimer's disease. Alzheimer's & Dementia: The Journal of the Alzheimer's Association, 5, 18–29. doi: 10.1016/j.jalz.2008.10.004.Google Scholar
Wang, Y. J., Zhou, H. D. and Zhou, X. F. (2006). Clearance of amyloid-beta in Alzheimer's disease: progress, problems and perspectives. Drug Discovery Today, 11, 931–938 Google Scholar
Xiang, Y. et al. (2015). Physiological amyloid-beta clearance in the periphery and its therapeutic potential for Alzheimer's disease. Acta Neuropathologia, 130, 487–499. doi: 10.1007/s00401-015-1477-1. Epub 2015 Sep 12.Google Scholar