Abstract
Abnormal processing of the amyloid precursor protein (APP) is thought to contribute to the formation of amyloid plaques in Alzheimer′s disease. Several studies suggest that inflammation, and possibly the cytokines released during the inflammatory process, may participate in the plaque formation. We have utilized a cell culture system to examine the effects of the cytokine interleukin-1β (IL-1β) on the processing of APP. We present data to show that IL-1β increases the maturation of APP and causes enhanced processing of the full length APP isoforms. In addition, as reported previously in HUVEC cells, IL-1β increases the secretion of APP in PC12 cells. Indomethacin and NDGA, reported inhibitors of the cyclooxygenase and lipoxygenase pathways, respectively, block these effects,suggesting the involvement of prostaglandins and leukotrienes in IL-1β mediated APP processing.
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