Świetlik Dariusz, Białowąs Jacek, Moryś Janusz, Klejbor Ilona, Kusiak Aida
Intrafaculty College of Medical Informatics and Biostatistics, Medical University of Gdańsk, 1 Debinki St., 80-211 Gdańsk, Poland.
Department of Anatomy and Neurobiology, Medical University of Gdańsk, 1 Debinki St., 80-211 Gdańsk, Poland.
Entropy (Basel). 2019 Jun 13;21(6):587. doi: 10.3390/e21060587.
The aim of this study was to evaluate the possibility of the gamma oscillation function (40-130 Hz) to reduce Alzheimer's disease related pathology in a computer model of the hippocampal network dentate gyrus, CA3, and CA1 (DG-CA3-CA1) regions. : Computer simulations were made for a pathological model in which Alzheimer's disease was simulated by synaptic degradation in the hippocampus. Pathology modeling was based on sequentially turning off the connections with entorhinal cortex layer 2 (EC2) and the dentate gyrus on CA3 pyramidal neurons. Gamma induction modeling consisted of simulating the oscillation provided by the septo-hippocampal pathway with band frequencies from 40-130 Hz. Pathological models with and without gamma induction were compared with a control. : In the hippocampal regions of DG, CA3, and CA1, and jointly DG-CA3-CA1 and CA3-CA1, gamma induction resulted in a statistically significant improvement in terms of increased numbers of spikes, spikes per burst, and burst duration as compared with the model simulating Alzheimer's disease (AD). The positive maximal Lyapunov exponent was negative in both the control model and the one with gamma induction as opposed to the pathological model where it was positive within the DG-CA3-CA1 region. Gamma induction resulted in decreased transfer entropy in accordance with the information flow in DG → CA3 and CA3 → CA1. : The results of simulation studies show that inducing gamma oscillations in the hippocampus may reduce Alzheimer's disease related pathology. Pathologically higher transfer entropy values after gamma induction returned to values comparable to the control model.
本研究的目的是在海马网络齿状回、CA3和CA1（DG-CA3-CA1）区域的计算机模型中评估伽马振荡功能（40-130赫兹）减轻阿尔茨海默病相关病理的可能性。：针对通过海马体突触退化模拟阿尔茨海默病的病理模型进行了计算机模拟。病理建模基于依次切断内嗅皮层第2层（EC2）与CA3锥体神经元上齿状回的连接。伽马诱导建模包括模拟由隔海马通路提供的40-130赫兹频段的振荡。将有和没有伽马诱导的病理模型与对照组进行比较。：在DG、CA3和CA1的海马区域，以及联合的DG-CA3-CA1和CA3-CA1区域，与模拟阿尔茨海默病（AD）的模型相比，伽马诱导在尖峰数量增加、每次爆发的尖峰数和爆发持续时间方面导致了统计学上显著的改善。对照模型和有伽马诱导的模型中的正最大李雅普诺夫指数均为负，而在DG-CA3-CA1区域内的病理模型中该指数为正。根据DG→CA3和CA3→CA1中的信息流，伽马诱导导致转移熵降低。：模拟研究结果表明，在海马体中诱导伽马振荡可能减轻阿尔茨海默病相关病理。伽马诱导后病理上较高的转移熵值恢复到与对照模型相当的值。
