Menzies Research Institute, University of Tasmania, Private Bag 24, Hobart, TAS 7001, Australia.
Neurochem Res. 2009 Oct;34(10):1824-9. doi: 10.1007/s11064-009-9960-5. Epub 2009 Apr 1.
The accumulation of oligomeric species of beta-amyloid protein in the brain is considered to be a key factor that causes Alzheimer's disease (AD). However, despite many years of research, the mechanism of neurotoxicity in AD remains obscure. Recent evidence strongly supports the theory that Ca2+ dysregulation is involved in AD. Amyloid proteins have been found to induce Ca2+ influx into neurons, and studies on transgenic mice suggest that this Ca2+ influx may alter neuronal excitability. The identification of a risk factor gene for AD that may be involved in the regulation of Ca2+ homeostasis and recent findings which suggest that presenilins may be involved in the regulation of intracellular Ca2+ stores provide converging lines of evidence that support the idea that Ca2+ dysregulation is a key step in the pathogenesis of AD.
β淀粉样蛋白寡聚物在大脑中的积累被认为是导致阿尔茨海默病（AD）的关键因素。然而，尽管经过多年的研究，AD 中的神经毒性机制仍然不清楚。最近的证据强烈支持钙稳态失调参与 AD 的理论。已发现淀粉样蛋白可诱导神经元内钙内流，并且对转基因小鼠的研究表明，这种钙内流可能改变神经元的兴奋性。AD 的风险因素基因的鉴定可能涉及钙稳态的调节，以及最近的研究结果表明早老素可能参与细胞内钙库的调节，这些都提供了支持钙稳态失调是 AD 发病机制中的关键步骤这一观点的证据。
