Long-term exposition of cells to β-amyloid results in decreased intracellular calcium concentration

András Palotás, J. Kálmán, Miklós Palotás, L. Kemény, Z. Janka, B. Penke

Research output: Contribution to journalArticle

7 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)543-547
Number of pages5
JournalNeurochemistry International
Volume42
Issue number7
DOIs
Publication statusPublished - Jun 2003

Fingerprint

Amyloid
Calcium
Peptides
Alzheimer Disease
Homeostasis
Fibroblasts

Keywords

  • β-Amyloid
  • Alzheimer's disease
  • Calcium
  • Calcium-antagonist
  • Fibroblast
  • Fluorimetry

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Cellular and Molecular Neuroscience

Cite this

Long-term exposition of cells to β-amyloid results in decreased intracellular calcium concentration. / Palotás, András; Kálmán, J.; Palotás, Miklós; Kemény, L.; Janka, Z.; Penke, B.

In: Neurochemistry International, Vol. 42, No. 7, 06.2003, p. 543-547.

Research output: Contribution to journalArticle

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