Investigating the Neural Correlates of Pathological Cortical Networks in Alzheimer's Disease Using Heterogeneous Neuronal Models

被引:16
作者
Abuhassan, Kamal [1 ]
Coyle, Damien [1 ,2 ]
Maguire, Liam P. [1 ,2 ]
机构
[1] Univ Ulster, Intelligent Syst Res Ctr, Derry BT48 7JL, North Ireland
[2] Univ Ulster, Sch Comp & Intelligent Syst, Derry BT48 7JL, North Ireland
关键词
Alzheimer's disease (AD); computational models; EEG; functional deficits; structural impairment; DECREASED EEG SYNCHRONIZATION; MILD COGNITIVE IMPAIRMENT; POTASSIUM CHANNELS; AMYLOID PEPTIDE; DYNAMICS; DEATH;
D O I
10.1109/TBME.2011.2181843
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
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 beta-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.
引用
收藏
页码:890 / 896
页数:7
相关论文
共 25 条
[1]  
Abuhassan K., 2011, P 33 ANN IEEE ENG ME, P2065
[2]  
Abuhassan K, 2011, IRISH J MED SCI, V180, P62
[3]  
[Anonymous], KYBERNETIK, DOI DOI 10.1007/BF00270757
[4]   Structure and function of kv4-family transient potassium channels [J].
Birnbaum, SG ;
Varga, AW ;
Yuan, LL ;
Anderson, AE ;
Sweatt, JD ;
Schrader, LA .
PHYSIOLOGICAL REVIEWS, 2004, 84 (03) :803-833
[5]  
Braitenberg V., 1991, ANATOMY CORTEX STAT
[6]   Neurofibrillary tangles and Alzheimer's disease [J].
Brion, JP .
EUROPEAN NEUROLOGY, 1998, 40 (03) :130-140
[7]   Forecasting the global burden of Alzheimer's disease [J].
Brookmeyer, Ron ;
Johnson, Elizabeth ;
Ziegler-Graham, Kathryn ;
Arrighi, H. Michael .
ALZHEIMERS & DEMENTIA, 2007, 3 (03) :186-191
[8]   Increased synchronization and decreased neural complexity underlie thalamocortical oscillatory dynamics in mild cognitive impairment [J].
Cantero, Jose L. ;
Atienza, Mercedes ;
Cruz-Vadell, Abel ;
Suarez-Gonzalez, Aida ;
Gil-Neciga, Eulogio .
NEUROIMAGE, 2009, 46 (04) :938-948
[9]   ALZHEIMERS-DISEASE - THE AMYLOID CASCADE HYPOTHESIS [J].
HARDY, JA ;
HIGGINS, GA .
SCIENCE, 1992, 256 (5054) :184-185
[10]   Spike-timing dynamics of neuronal groups [J].
Izhikevich, EM ;
Gally, JA ;
Edelman, GM .
CEREBRAL CORTEX, 2004, 14 (08) :933-944