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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicity.
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Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicity.

机译：星形胶质细胞中细胞内钙和谷胱甘肽的变化是淀粉样蛋白神经毒性的主要机制。

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摘要

Although the accumulation of the neurotoxic peptide beta amyloid (betaA) in the CNS is a hallmark of Alzheimer's disease, the mechanism of betaA neurotoxicity remains controversial. In cultures of mixed neurons and astrocytes, we found that both the full-length peptide betaA (1-42) and the neurotoxic fragment (25-35) caused sporadic cytoplasmic calcium [intracellular calcium ([Ca2+]c)] signals in astrocytes that continued for hours, whereas adjacent neurons were completely unaffected. Nevertheless, after 24 hr, although astrocyte cell death was marginally increased, approximately 50% of the neurons had died. The [Ca2+]c signal was entirely dependent on Ca2+ influx and was blocked by zinc and by clioquinol, a heavy-metal chelator that is neuroprotective in models of Alzheimer's disease. Neuronal death was associated with Ca2+-dependent glutathione depletion in both astrocytes and neurons. Thus, astrocytes appear to be the primary target of betaA, whereas the neurotoxicity reflects the neuronal dependence on astrocytes for antioxidant support.
机译：尽管中枢神经系统中神经毒性肽β淀粉样蛋白（betaA）的积累是阿尔茨海默氏病的标志，但betaA神经毒性的机制仍存在争议。在混合神经元和星形胶质细胞的培养物中，我们发现全长肽betaA（1-42）和神经毒性片段（25-35）均会在星形胶质细胞中引起偶发的细胞质钙[胞内钙（[Ca2 +] c）]信号，持续数小时，而相邻的神经元完全不受影响。尽管如此，在24小时后，尽管星形胶质细胞死亡略有增加，但约有50％的神经元已经死亡。 [Ca2 +] c信号完全取决于Ca2 +的流入，并被锌和重金属螯合剂Clioquinol所阻断，Clioquinol是一种重金属螯合剂，在阿尔茨海默氏病模型中具有神经保护作用。神经元死亡与星形胶质细胞和神经元中钙依赖的谷胱甘肽耗竭有关。因此，星形胶质细胞似乎是betaA的主要目标，而神经毒性反映了神经元对星形胶质细胞的抗氧化剂支持。

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