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Expression of interleukin-18 is increased in the brains of Alzheimer's disease patients
Department of Neuroscience and Neurology, University of Kuopio Finland. (Alafuzoff)
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2009 (English)In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 30, no 2, 198-209 p.Article in journal (Refereed) Published
Abstract [en]

The inflammatory cytokines can initiate nerve cell degeneration and enhance the plaque production typically found in Alzheimer's disease (AD). Interleukin-18 (IL-18) is an inflammatory cytokine, which can induce the expression of interferon-gamma. This interleukin shares similarities with the IL-1 family of proteins. Like IL-1 beta, IL-18 is cleaved by caspase-1 (ICE) to an active secreted form. We examined the expressions of IL-18, -1 beta and ICE in different brain regions from AD patients that were categorized with respect to the Braak stage, and age-matched with non-demented controls. The levels of total-RNA and protein of IL-18 and ICE were increased, especially in the frontal lobe of AD patients and this change was not modified by ApoE genotype. Immunohistochemistry of AD brain samples detected IL-18 in microglia, astrocytes, and surprisingly in neurons, and it is also co-localized not only with amyloid-beta plaques but also with tau. In CSF, elevated IL-18 level was detected only in men and it also correlated with CSF tau in MCI. IL-18 may thus be a potential biomarker for men. Plasma levels of IL-18 showed no correlation with the disease. In conclusion, amyloid-beta may induce the synthesis of IL-18, and IL-18 kinases involved in tau phosphorylation as a part of the amyloid-associated inflammatory reaction.

Place, publisher, year, edition, pages
2009. Vol. 30, no 2, 198-209 p.
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Research subject
Pathology; Neurology
URN: urn:nbn:se:uu:diva-153117DOI: 10.1016/j.neurobiolaging.2007.06.006PubMedID: 17658666OAI: oai:DiVA.org:uu-153117DiVA: diva2:415249
Available from: 2011-05-06 Created: 2011-05-06 Last updated: 2016-05-13

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