| First Author | Ojala J | Year | 2009 |
| Journal | Neurobiol Aging | Volume | 30 |
| Issue | 2 | Pages | 198-209 |
| PubMed ID | 17658666 | Mgi Jnum | J:145816 |
| Mgi Id | MGI:3836111 | Doi | 10.1016/j.neurobiolaging.2007.06.006 |
| Citation | Ojala J, et al. (2009) Expression of interleukin-18 is increased in the brains of Alzheimer's disease patients. Neurobiol Aging 30(2):198-209 |
| abstractText | 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. |
