Virtual Therapy with the NMDA Antagonist Memantine in Hippocampal Models of Moderate to Severe Alzheimer's Disease, in Silico Trials.

The variability in clinical trial results on memantine treatment of Alzheimer's disease remains incompletely explained. The aim of this in silico study is a virtual memantine therapy for Alzheimer's disease that provides a different perspective on clinical trials; An in silico randomised trial using virtual hippocampi to treat moderate to severe Alzheimer's disease with doses of memantine 3-30 µM compared to placebo. The primary endpoint was the number of impulses (spikes).

The Computer Simulation of Therapy with the NMDA Antagonist in Excitotoxic Neurodegeneration in an Alzheimer's Disease-like Pathology.

(1) Background: The use of uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists results in neuroprotective benefits in patients with moderate to severe Alzheimer’s disease. In this study, we demonstrated mathematical and computer modelling of the excitotoxicity phenomenon and performed virtual memantine therapy. (2) Methods: A computer simulation environment of the N-methyl-D-aspartate receptor combining biological mechanisms of channel activation by means of excessive extracellular glutamic acid concentration in three models of excitotoxicity severity.

Effects of Inducing Gamma Oscillations in Hippocampal Subregions DG, CA3, and CA1 on the Potential Alleviation of Alzheimer's Disease-Related Pathology: Computer Modeling and Simulations.

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.

Computer Modeling of Alzheimer's Disease-Simulations of Synaptic Plasticity and Memory in the CA3-CA1 Hippocampal Formation Microcircuit.

This paper aims to present computer modeling of synaptic plasticity and memory in the CA3-CA1 hippocampal formation microcircuit. The computer simulations showed a comparison of a pathological model in which Alzheimer's disease (AD) was simulated by synaptic degradation in the hippocampus and control model (healthy) of CA3-CA1 networks with modification of weights for the memory. There were statistically higher spike values of both CA1 and CA3 pyramidal cells in the control model than in the pathological model (p = 0.

Computer Model of Synapse Loss During an Alzheimer's Disease-Like Pathology in Hippocampal Subregions DG, CA3 and CA1-The Way to Chaos and Information Transfer.

The aim of the study was to compare the computer model of synaptic breakdown in an Alzheimer's disease-like pathology in the dentate gyrus (DG), CA3 and CA1 regions of the hippocampus with a control model using neuronal parameters and methods describing the complexity of the system, such as the correlative dimension, Shannon entropy and positive maximal Lyapunov exponent. The model of synaptic breakdown (from 13% to 50%) in the hippocampus modeling the dynamics of an Alzheimer's disease-like pathology was simulated. Modeling consisted in turning off one after the other EC2 connections and connections from the dentate gyrus on the CA3 pyramidal neurons.

Application of Artificial Neural Networks to Identify Alzheimer's Disease Using Cerebral Perfusion SPECT Data.

The aim of this study was to demonstrate the usefulness of artificial neural networks in Alzheimer disease diagnosis (AD) using data of brain single photon emission computed tomography (SPECT). The results were compared with discriminant analysis. The study population consisted of 132 clinically diagnosed patients.