Alpha and Theta Rhythm Abnormality in Alzheimer's Disease: A Study Using a Computational Model
Alpha and Theta Rhythm Abnormality in Alzheimer's Disease: A Study Using a Computational Model
复制标题
DOI：
10.1007/978-1-4614-0164-3_6
复制
发表时间：
2011-01-01
期刊：
影响因子：
--
通讯作者：
Maguire, Liam P.
中科院分区：
文献类型：
--
作者：
Bhattacharya, Basabdatta Sen;Coyle, Damien;Maguire, Liam P.
对阿尔茨海默病（AD）患者的脑电图（EEG）研究显示α频带（7.5-13 Hz）内的平均功率衰减和θ频带（4-7 Hz）中的功率增加。大量证据表明，丘脑皮层回路支持α和θ节律的产生和调制。本章中介绍的研究旨在更好地了解AD中EEG频带功率变化的神经机制，这可能在未来为疾病的早期检测和神经药物研究提供有用的生物标志物。该研究基于丘脑皮质回路的经典计算模型，该模型在theta和alpha频段内表现出振荡。我们感兴趣的是模型振荡行为的变化与丘脑皮层以及感觉输入途径的连接参数的变化。的突触组织以及模型中的连接参数值进行修改的基础上最近的实验数据从猫丘脑。我们观察到，在模型中的抑制人口起着至关重要的作用，在调解的振荡行为的模型输出。此外，在传入和传出通路的抑制性人口的连接参数的增加引起的输出功率谱的放缓。这些观察结果可能对扩展该模型进行进一步的AD研究具有影响。
Electroencephalography (EEG) studies in Alzheimer's Disease (AD) patients show an attenuation of average power within the alpha band (7.5-13 Hz) and an increase of power in the theta band (4-7 Hz). Significant body of evidence suggest that thalamocortical circuitry underpin the generation and modulation of alpha and theta rhythms. The research presented in this chapter is aimed at gaining a better understanding of the neuronal mechanisms underlying EEG band power changes in AD which may in the future provide useful biomarkers towards early detection of the disease and for neuropharmaceutical investigations. The study is based on a classic computational model of the thalamocortical circuitry which exhibits oscillation within the theta and the alpha bands. We are interested in the change in model oscillatory behaviour corresponding with changes in the connectivity parameters in the thalamocortical as well as sensory input pathways. The synaptic organisation as well as the connectivity parameter values in the model are modified based on recent experimental data from the cat thalamus. We observe that the inhibitory population in the model plays a crucial role in mediating the oscillatory behaviour of the model output. Further, increase in connectivity parameters in the afferent and efferent pathways of the inhibitory population induces a slowing of the output power spectra. These observations may have implications for extending the model for further AD research.