Etcheberrigaray R, Payne J L, Alkon D L
Institute for Cognitive and Computational Sciences, Georgetown University Medical Center, Washington, DC, USA.
Life Sci. 1996;59(5-6):491-8. doi: 10.1016/0024-3205(96)00328-1.
It has been shown that K+ channels, Cp20 (a 20kD GTP-binding protein), and intracellular calcium release, play a key role in associative memory storage. These same elements have been shown to be altered in fibroblasts from Alzheimer's Disease (AD) patients. In addition, it has been shown that PKC, also implicated in memory storage and closely related to the above mentioned components, is also altered in AD fibroblasts. Moreover, beta-amyloid was capable of inducing an AD-like phenotype for K+ channels and Cp20 in otherwise normal fibroblasts, providing additional evidence for the potential involvement of these components in AD and suggesting a possible pathological consequence of soluble beta-amyloid elevation in AD. Preliminary evidence shows that comparable changes in potassium channel function are also present in human olfactory neuroblasts from AD patients. These results indicate that the observed changes not only occur in peripheral tissues such as fibroblasts, but also in neural tissue, the primary site of AD pathology.
已表明钾离子通道、Cp20（一种20kD的GTP结合蛋白）以及细胞内钙释放，在联合记忆存储中起关键作用。这些相同的元件在阿尔茨海默病（AD）患者的成纤维细胞中已被证明发生了改变。此外，已表明蛋白激酶C（PKC）也与记忆存储有关且与上述成分密切相关，在AD成纤维细胞中也发生了改变。而且，β-淀粉样蛋白能够在原本正常的成纤维细胞中诱导钾离子通道和Cp20出现类似AD的表型，为这些成分可能参与AD提供了额外证据，并提示了AD中可溶性β-淀粉样蛋白升高可能的病理后果。初步证据表明，AD患者的人嗅神经母细胞中也存在钾通道功能的类似变化。这些结果表明，观察到的变化不仅发生在成纤维细胞等外周组织中，也发生在神经组织中，而神经组织是AD病理的主要部位。
