School of Computer Science, University of Birmingham Birmingham, UK.
Front Comput Neurosci. 2012 Jan 18;6:2. doi: 10.3389/fncom.2012.00002. eCollection 2012.
This work models the progression of beta-amyloid pathology according to Small's synaptic scaling theory in an updated version of Ruppin and Reggia's associative neural network model of Alzheimer's disease, leading to a self-reinforcing cascade of damage. Using an information theoretic approach, it is shown that the simulated beta-amyloid pathology initially selectively targets neurons with low informational contribution to the overall performance of the network, but that it targets neurons with increasingly higher significance to the network as the disease progresses. The results additionally provide a possible explanation for the apparent low correlation between amyloid plaque density and cognitive decline in the early stages of Alzheimer's disease.
这项工作根据 Small 的突触缩放理论,在 Ruppin 和 Reggia 的阿尔茨海默病关联神经网络模型的更新版本中对β-淀粉样蛋白病理进行建模,导致自我强化的损伤级联。使用信息论方法,结果表明,模拟的β-淀粉样蛋白病理最初选择性地针对对网络整体性能贡献较低的神经元,但随着疾病的进展,针对对网络具有越来越高意义的神经元。此外,该结果还为阿尔茨海默病早期淀粉样斑块密度与认知能力下降之间明显低相关性提供了一种可能的解释。