Intelligent Systems Research Centre, University of Ulster, Derry, UK.
IEEE Trans Biomed Eng. 2012 Mar;59(3):890-6. doi: 10.1109/TBME.2011.2181843. Epub 2011 Dec 26.
This paper describes an investigation into the pathophysiological causes of abnormal cortical oscillations in Alzheimer's disease (AD) using two heterogeneous neuronal network models. The effect of excitatory circuit disruption on the beta band power (13-30 Hz) using a conductance-based network model of 200 neurons is assessed. Then, the neural correlates of abnormal cortical oscillations in different frequency bands based on a larger network model of 1000 neurons consisting of different types of cortical neurons are also analyzed. EEG studies in AD patients have shown that beta band power (13-30 Hz) decreased in the early stages of the disease with a parallel increase in theta band power (4-7 Hz). This abnormal change progresses with the later stages of the disease but with decreased power spectra in other fast frequency bands plus an increase in delta band power (1-3 Hz). Our results show that, despite the heterogeneity of the network models, the beta band power is significantly affected by excitatory neural and synaptic loss. Second, the results of modeling a functional impairment in the excitatory circuit shows that beta band power exhibits the most decrease compared with other bands. Previous biological experiments on different types of cultural excitatory neurons show that cortical neuronal death is mediated by dysfunctional ionic behavior that might specifically contribute to the pathogenesis of β-amyloid-peptide-induced neuronal death in AD. Our study also shows that beta band power was the first affected component when the modeled excitatory circuit begins to lose neurons and synapses.
本文使用两个异质神经元网络模型研究了阿尔茨海默病(AD)中皮质振荡异常的病理生理原因。评估了基于电导的 200 个神经元网络模型中兴奋性电路破坏对β频段功率(13-30Hz)的影响。然后,还分析了基于由不同类型皮质神经元组成的 1000 个神经元更大网络模型的不同频段异常皮质振荡的神经相关性。AD 患者的 EEG 研究表明,β频段功率(13-30Hz)在疾病早期降低,同时θ频段功率(4-7Hz)增加。这种异常变化随着疾病的后期进展而发展,但在其他快速频段的功率谱降低,同时δ频段功率(1-3Hz)增加。我们的研究结果表明,尽管网络模型存在异质性,但β频段功率仍受到兴奋性神经和突触损失的显著影响。其次,对兴奋性电路功能障碍进行建模的结果表明,与其他频段相比,β频段功率下降幅度最大。针对不同类型兴奋性神经元的先前生物学实验表明,皮质神经元死亡是由功能失调的离子行为介导的,这可能是 AD 中β-淀粉样肽诱导的神经元死亡发病机制的特定贡献因素。我们的研究还表明,当模拟的兴奋性电路开始失去神经元和突触时,β 频段功率是第一个受到影响的成分。