β-amyloid (Aβ) is toxic to cells and has been identified as the major participant in the pathogenesis of Alzheimer's disease. In both the corpus luteum organ culture model of apoptosis and in neuronal cells, Aβ was able to mimic the action of superoxide dismutase and prevent apoptotic endonucleolytic DNA fragmentation at low concentrations. Furthermore the longer form of Aβ (Aβ 1-42) was more potent than Aβ 1-40 in reducing apoptosis. At increasing Aβ concentrations a loss of anti-apoptotic activity became evident. In addition, the anti-apoptotic effect of Aβ was dependent upon copper binding to the peptide. Since copper is a transition metal and is integral to the activity of the superoxide dismutase enzyme, it is suggested that the novel anti-apoptotic effect of Aβ may be mediated by superoxide dismutase-like activity.
|Number of pages||7|
|Publication status||Published - 1999|