Fraser S P, Suh Y H, Djamgoz M B
Dept of Biology, Imperial College of Science, Technology and Medicine, London, UK.
Trends Neurosci. 1997 Feb;20(2):67-72. doi: 10.1016/s0166-2236(96)10079-5.
Alzheimer's disease is a progressive dementia characterized in part by deposition of proteinaceous plaques in various areas of the brain. The main plaque protein component is beta-amyloid, a metabolic product of the beta-amyloid precursor protein. Substantial evidence has implicated beta-amyloid (and other amyloidogenic fragments of the precursor protein) with the neurodegeneration observed in Alzheimer's disease. Recently, beta-amyloid precursor protein and its amyloidogenic metabolic fragments have been shown to alter cellular ionic activity, either through interaction with existing channels or by de novo channel formation. Such alteration in ionic homeostasis has also been linked with cellular toxicity and might provide a molecular mechanism underlying the neurodegeneration seen in Alzheimer's disease.
阿尔茨海默病是一种进行性痴呆，其部分特征是在大脑的各个区域出现蛋白质斑块沉积。主要的斑块蛋白成分是β-淀粉样蛋白，它是β-淀粉样前体蛋白的代谢产物。大量证据表明，β-淀粉样蛋白（以及前体蛋白的其他淀粉样生成片段）与阿尔茨海默病中观察到的神经退行性变有关。最近，β-淀粉样前体蛋白及其淀粉样生成代谢片段已被证明可通过与现有通道相互作用或通过从头形成通道来改变细胞离子活性。离子稳态的这种改变也与细胞毒性有关，可能为阿尔茨海默病中所见的神经退行性变提供分子机制。
