Institution: | a Department of Medical Chemistry, University of Szeged, H-6721 Szeged, Dóm tér 8, Hungary b Department of Psychiatry, University of Szeged, H-6721 Szeged, Semmelweis u. 6, Hungary c Department of Dermatology, University of Szeged, H-6721 Szeged, Korányi fasor 6, Hungary |
Abstract: | The ubiquitously present β-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 β-amyloid has, in deed, 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, β-amyloid has biphasic effects: acutely, it increases the calcium-concentration of cells; in contrast, on the long-run, β-amyloid peptide acts as a calcium-antagonist. Therefore, the idea that β-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. |