Division of Biostatistics and Neural Networks, Medical University of Gdańsk, Dębinki 1, 80-211 Gdańsk, Poland.
Department of Periodontology and Oral Mucosa Diseases, Medical University of Gdańsk, 80-204 Gdańsk, Poland.
Int J Environ Res Public Health. 2022 Apr 14;19(8):4727. doi: 10.3390/ijerph19084727.
(1) Background: in patients with neurodegenerative diseases, noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists provide neuroprotective advantages. We performed memantine therapy and proved mathematical and computer modeling of neurodegenerative disease in this study. (2) Methods: a computer simulation environment of the N-methyl-D-aspartate receptor incorporating biological mechanisms of channel activation by high extracellular glutamic acid concentration. In comparison to controls, pathological models were essentially treated with doses of memantine 3−30 µM. (3) Results: the mean values and 95% CI for Shannon entropy in Alzheimer’s disease (AD) and memantine treatment models were 1.760 (95% CI, 1.704−1.818) vs. 2.385 (95% CI, 2.280−2.490). The Shannon entropy was significantly higher in the memantine treatment model relative to AD model (p = 0.0162). The mean values and 95% CI for the positive Lyapunov exponent in AD and memantine treatment models were 0.125 (95% CI, NE−NE) vs. 0.058 (95% CI, 0.044−0.073). The positive Lyapunov exponent was significantly higher in the AD model relative to the memantine treatment model (p = 0.0091). The mean values and 95% CI for transfer entropy in AD and memantine treatment models were 0.081 (95% CI, 0.048−0.114) vs. 0.040 (95% CI, 0.019−0.062). The transfer entropy was significantly higher in the AD model relative to the memantine treatment model (p = 0.0146). A correlation analysis showed positive and statistically significant correlations of the memantine concentrations and the positive Lyapunov exponent (correlation coefficient R = 0.87, p = 0.0023) and transfer entropy (TE) (correlation coefficient R = 0.99, p < 0.000001). (4) Conclusions: information theory results of simulation studies show that the NMDA antagonist, memantine, causes neuroprotective benefits in patients with AD. Our simulation study opens up remarkable new scenarios in which a medical product, drug, or device, can be developed and tested for efficacy based on parameters of information theory.
（1）背景：在神经退行性疾病患者中，非竞争性 N-甲基-D-天冬氨酸（NMDA）受体拮抗剂提供神经保护优势。我们在这项研究中进行了美金刚治疗，并证明了神经退行性疾病的数学和计算机建模。（2）方法：一个包含高细胞外谷氨酸浓度激活通道的生物学机制的 NMDA 受体计算机模拟环境。与对照组相比，病理模型主要用 3-30µM 的美金刚剂量治疗。（3）结果：阿尔茨海默病（AD）和美金刚治疗模型的香农熵平均值和 95%置信区间分别为 1.760（95%置信区间，1.704-1.818）和 2.385（95%置信区间，2.280-2.490）。美金刚治疗模型的香农熵明显高于 AD 模型（p=0.0162）。AD 和美金刚治疗模型的正 Lyapunov 指数平均值和 95%置信区间分别为 0.125（95%置信区间，NE-NE）和 0.058（95%置信区间，0.044-0.073）。AD 模型的正 Lyapunov 指数明显高于美金刚治疗模型（p=0.0091）。AD 和美金刚治疗模型的传递熵平均值和 95%置信区间分别为 0.081（95%置信区间，0.048-0.114）和 0.040（95%置信区间，0.019-0.062）。AD 模型的传递熵明显高于美金刚治疗模型（p=0.0146）。相关性分析显示，美金刚浓度与正 Lyapunov 指数（相关系数 R=0.87，p=0.0023）和传递熵（TE）（相关系数 R=0.99，p<0.000001）呈正相关且具有统计学意义。（4）结论：模拟研究的信息论结果表明，NMDA 拮抗剂美金刚可使 AD 患者受益于神经保护。我们的模拟研究开辟了新的途径，可以根据信息论参数开发和测试治疗疾病的药物、药物或设备。
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