Department of Clinical Neurophysiology and MEG, VU University Medical Center, Amsterdam, The Netherlands.
PLoS Comput Biol. 2012;8(8):e1002582. doi: 10.1371/journal.pcbi.1002582. Epub 2012 Aug 16.
Brain connectivity studies have revealed that highly connected 'hub' regions are particularly vulnerable to Alzheimer pathology: they show marked amyloid-β deposition at an early stage. Recently, excessive local neuronal activity has been shown to increase amyloid deposition. In this study we use a computational model to test the hypothesis that hub regions possess the highest level of activity and that hub vulnerability in Alzheimer's disease is due to this feature. Cortical brain regions were modeled as neural masses, each describing the average activity (spike density and spectral power) of a large number of interconnected excitatory and inhibitory neurons. The large-scale network consisted of 78 neural masses, connected according to a human DTI-based cortical topology. Spike density and spectral power were positively correlated with structural and functional node degrees, confirming the high activity of hub regions, also offering a possible explanation for high resting state Default Mode Network activity. 'Activity dependent degeneration' (ADD) was simulated by lowering synaptic strength as a function of the spike density of the main excitatory neurons, and compared to random degeneration. Resulting structural and functional network changes were assessed with graph theoretical analysis. Effects of ADD included oscillatory slowing, loss of spectral power and long-range synchronization, hub vulnerability, and disrupted functional network topology. Observed transient increases in spike density and functional connectivity match reports in Mild Cognitive Impairment (MCI) patients, and may not be compensatory but pathological. In conclusion, the assumption of excessive neuronal activity leading to degeneration provides a possible explanation for hub vulnerability in Alzheimer's disease, supported by the observed relation between connectivity and activity and the reproduction of several neurophysiologic hallmarks. The insight that neuronal activity might play a causal role in Alzheimer's disease can have implications for early detection and interventional strategies.
脑连接研究表明,高度连接的“枢纽”区域特别容易受到阿尔茨海默病病理的影响:它们在早期就表现出明显的淀粉样蛋白-β沉积。最近,过度的局部神经元活动已被证明会增加淀粉样蛋白的沉积。在这项研究中,我们使用计算模型来检验以下假设:枢纽区域具有最高水平的活动,而阿尔茨海默病中的枢纽易损性是由于这一特征。皮质脑区被建模为神经团,每个神经团描述大量相互连接的兴奋性和抑制性神经元的平均活动(尖峰密度和频谱功率)。大规模网络由 78 个神经团组成,根据基于人类 DTI 的皮质拓扑结构连接。尖峰密度和频谱功率与结构和功能节点度呈正相关,证实了枢纽区域的高活动,也为高静息状态默认模式网络活动提供了可能的解释。“活动依赖的退化”(ADD)是通过将突触强度降低为主要兴奋性神经元的尖峰密度的函数来模拟的,并与随机退化进行比较。使用图论分析评估了由此产生的结构和功能网络变化。ADD 的影响包括振荡减慢、频谱功率损失和长程同步、枢纽易损性以及功能网络拓扑的破坏。观察到的尖峰密度和功能连接的短暂增加与轻度认知障碍(MCI)患者的报告相匹配,并且可能不是代偿性的而是病理性的。总之,过度神经元活动导致退化的假设为阿尔茨海默病中的枢纽易损性提供了可能的解释,这与观察到的连接性和活动之间的关系以及几个神经生理标志的再现相吻合。神经元活动可能在阿尔茨海默病中起因果作用的观点可能对早期检测和干预策略具有重要意义。