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

被引：9

作者：

Palotás, A

Kálmán, J

Palotás, M

Kemény, L

Janka, Z

Penke, O

机构：

[1] Univ Szeged, Dept Med Chem, H-6721 Szeged, Hungary

[2] Univ Szeged, Dept Psychiat, H-6721 Szeged, Hungary

[3] Univ Szeged, Dept Dermatol, H-6721 Szeged, Hungary

来源：

NEUROCHEMISTRY INTERNATIONAL | 2003年 / 42卷 / 07期

关键词：

Alzheimer's disease; beta-amyloid; fibroblast; calcium; fluorimetry; calcium-antagonist; ALZHEIMERS-DISEASE; HIPPOCAMPAL-NEURONS; PRECURSOR PROTEIN; RAT ASTROCYTES; FIBROBLASTS; ACTIVATION; CA2+; GLUTAMATE; RECEPTORS; DEMENTIA;

D O I：

10.1016/S0197-0186(02)00188-2

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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, 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, 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. (C) 2003 Elsevier Science Ltd. All rights reserved.

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页码：543 / 547

页数：5

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