2658-6533Research Results in Biomedicine2658-653310.18413/2658-6533-2025-11-4-0-73942PharmacologyExperimental model of Alzheimer's disease caused by intrahippocampal injection of sodium azide. Comparability with the amyloid modelExperimental model of Alzheimer's disease caused by intrahippocampal injection of sodium azide. Comparability with the amyloid modelPozdnyakovDmitry I.PozdnyakovDmitry I.pozdniackow.dmitry@yandex.ru202511400

Background: The treatment of Alzheimer's disease is currently a complex medical task, requiring constant research and development of new medicines. This raises the question of choosing a relevant experimental model of Alzheimer's disease. The aim of the study: To conduct a comparative evaluation of two interventional experimental models of Alzheimer's disease: induced by the injection of beta-amyloid fragments and induced by the sodium azide injection. Materials and methods: Alzheimer's disease was modeled by injection of beta-amyloid fragments 1-42 (1 mmol/L) or sodium azide solutions (1M, 2M, 3M and 4M concentrations) into the CA1 part of the hippocampus of male Wistar rats. After 60 days, the animals were evaluated for changes in cognitive functions in the Y-maze test. Changes in the concentration of phosphorylated tau-protein, apoptosis-inducing factor, aerobic and anaerobic metabolism reactions, superoxidedismutase activity and thiobarbituric acid reactive substances were determined in the hippocampal tissue. The obtained results statistically were processed using the StatPlus 7.0 software. Results: The study showed that the injection of sodium azide in concentrations of 3M and 4M into the hippocampus of animals, as well as fragments of β-amyloid, contributes to the development of cognitive deficits comparable in severity, increases the concentration of tau-protein in hippocampal tissue by 4.1, 3.9 and 4.7 times (all indicators p<0.05 relative to untreated animals), respectively. Also, injection of 3M and 4M solutions of sodium azide into the hippocampus of rats, as well as fragments of β-amyloid, an increase in the content of apoptosis-inducing factor in 3.5 (p<0.05); 3.4 (p<0.05) and 4.0 times (p<0.05), respectively, accompanied by inhibition of aerobic metabolism and activation of anaerobic one, and oxidative stress also. Injecting sodium azide at concentrations of 1M and 2M resulted in significantly smaller changes than injecting 3M and 4M solutions of sodium azide and beta-amyloid fragments. Conclusion: The experimental models of Alzheimer's disease analyzed in the course of this work demonstrate the formation of comparable pathogenetic changes, while the optimal concentration of sodium azide for inducing Alzheimer's disease can be considered 3M or 4M

Background: The treatment of Alzheimer's disease is currently a complex medical task, requiring constant research and development of new medicines. This raises the question of choosing a relevant experimental model of Alzheimer's disease. The aim of the study: To conduct a comparative evaluation of two interventional experimental models of Alzheimer's disease: induced by the injection of beta-amyloid fragments and induced by the sodium azide injection. Materials and methods: Alzheimer's disease was modeled by injection of beta-amyloid fragments 1-42 (1 mmol/L) or sodium azide solutions (1M, 2M, 3M and 4M concentrations) into the CA1 part of the hippocampus of male Wistar rats. After 60 days, the animals were evaluated for changes in cognitive functions in the Y-maze test. Changes in the concentration of phosphorylated tau-protein, apoptosis-inducing factor, aerobic and anaerobic metabolism reactions, superoxidedismutase activity and thiobarbituric acid reactive substances were determined in the hippocampal tissue. The obtained results statistically were processed using the StatPlus 7.0 software. Results: The study showed that the injection of sodium azide in concentrations of 3M and 4M into the hippocampus of animals, as well as fragments of β-amyloid, contributes to the development of cognitive deficits comparable in severity, increases the concentration of tau-protein in hippocampal tissue by 4.1, 3.9 and 4.7 times (all indicators p<0.05 relative to untreated animals), respectively. Also, injection of 3M and 4M solutions of sodium azide into the hippocampus of rats, as well as fragments of β-amyloid, an increase in the content of apoptosis-inducing factor in 3.5 (p<0.05); 3.4 (p<0.05) and 4.0 times (p<0.05), respectively, accompanied by inhibition of aerobic metabolism and activation of anaerobic one, and oxidative stress also. Injecting sodium azide at concentrations of 1M and 2M resulted in significantly smaller changes than injecting 3M and 4M solutions of sodium azide and beta-amyloid fragments. Conclusion: The experimental models of Alzheimer's disease analyzed in the course of this work demonstrate the formation of comparable pathogenetic changes, while the optimal concentration of sodium azide for inducing Alzheimer's disease can be considered 3M or 4M

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