Long-term exposition of cells to beta-amyloid results in decreased intracellular calcium concentration.
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.
Palotás
András
A
Department of Medical Chemistry, University of Szeged, H-6721 Szeged, Dóm tér 8, Hungary. palotas@nepsy.szote.u-szaged.hu
Kálmán
János
J
Palotás
Miklós
M
Kemény
Lajos
L
Janka
Zoltán
Z
Penke
Botond
B
D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism*; D005542:Forearm; D006801:Humans; D007425:Intracellular Membranes / Q000378:metabolism*; D009994:Osmolar Concentration; D012867:Skin / Q000166:cytology; D013997:Time Factors
D016229:Amyloid beta-Peptides; D002118:Calcium