The ubiquitously present beta-amyloid peptide plays an important role in the pathogenesis of Alzheimer's disease. Its neurotoxicity has been blamed on its mal-activity to increase calcium-levels. In the present study, we demonstrate that treatment of fibroblasts with beta-amyloid has, indeed, resulted in a transient rise in the calcium-concentration. Chronic exposition of cultures to the peptide, however, caused a fall in the calcium-level. Apparently, beta-amyloid has biphasic effects: acutely, it increases the calcium-concentration of cells; in contrast, on the long-run, beta-amyloid peptide acts as a calcium-antagonist. Therefore, the idea that beta-amyloid peptide leads to neural degeneration solely by increasing cells' calcium concentration must be replaced with a more complex view of its dual function in intracellular ionic homeostasis.