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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Long-term exposition of cells to beta-amyloid results in decreased intracellular calcium concentration.
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Long-term exposition of cells to beta-amyloid results in decreased intracellular calcium concentration.

机译：细胞长期暴露于β-淀粉样蛋白会导致细胞内钙浓度降低。

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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, 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.
机译：普遍存在的β-淀粉样肽在阿尔茨海默氏病的发病机理中起重要作用。其神经毒性被归因于其不良活动以增加钙水平。在本研究中，我们证明用β-淀粉样蛋白处理成纤维细胞确实导致钙浓度的短暂升高。然而，将培养物长期暴露于该肽会导致钙水平下降。显然，β-淀粉样蛋白具有双相作用：急性地，它增加了细胞的钙浓度;相反，从长远来看，β-淀粉样蛋白肽可作为钙拮抗剂。因此，仅通过增加细胞钙浓度导致β-淀粉样蛋白肽导致神经退行性变的观点必须用更复杂的观点来代替，即其在细胞内离子稳态中的双重功能。

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