<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>19(8)</volume><submitter>Swietlik D</submitter><pubmed_abstract>(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 significant</pubmed_abstract><journal>International journal of environmental research and public health</journal><pagination>4727</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9027074</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Computational Modeling of Therapy with the NMDA Antagonist in Neurodegenerative Disease: Information Theory in the Mechanism of Action of Memantine.</pubmed_title><pmcid>PMC9027074</pmcid><pubmed_authors>Kusiak A</pubmed_authors><pubmed_authors>Ossowska A</pubmed_authors><pubmed_authors>Swietlik D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Computational Modeling of Therapy with the NMDA Antagonist in Neurodegenerative Disease: Information Theory in the Mechanism of Action of Memantine.</name><description>(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 significant</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2025-04-05T13:23:50.188Z</modification><creation>2025-04-05T13:23:50.188Z</creation></dates><accession>S-EPMC9027074</accession><cross_references><pubmed>35457595</pubmed><doi>10.3390/ijerph19084727</doi></cross_references></HashMap>