Ionic effects of the Alzheimer's disease beta-amyloid precursor protein and its metabolic fragments
Ionic effects of the Alzheimer's disease beta-amyloid precursor protein and its metabolic fragments
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DOI：
10.1016/s0166-2236(96)10079-5
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发表时间：
1997-02-01
影响因子：
15.9
通讯作者：
Djamgoz, MBA
中科院分区：
文献类型：
--
作者：
Fraser, SP;Suh, YH;Djamgoz, MBA
阿尔茨海默病是一种进行性痴呆，其部分特征是大脑不同区域的蛋白斑块沉积。斑块蛋白的主要成分是β -淀粉样蛋白，是β -淀粉样蛋白前体蛋白的代谢产物。大量证据表明-淀粉样蛋白（和其他淀粉样前体蛋白片段）与阿尔茨海默病中观察到的神经变性有关。最近，β -淀粉样蛋白前体蛋白及其淀粉样代谢片段已被证明可以通过与现有通道的相互作用或通过重新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，并可能提供阿尔茨海默病神经退行性变的分子机制。
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.