Nevmerzhytska N. M.

CHARACTERIZATION OF AZIDE-INDUCED EXPERIMENTAL DEMENTIA OF THE ALZHEIMER'S TYPE

---

Show/Download

About the author:

Nevmerzhytska N. M.

Heading:

MODERN MEDICAL ACHIEVEMENTS

Type of article:

Scientific article

Annotation:

Dementia is a syndrome caused by the presence of organic damage to the brain, the main manifestations of which are severe cognitive disorders and impaired self-care. This syndrome occurs in many nosologies: cerebrovascular diseases, Alzheimer's disease, Pick's disease, Gentinckton's disease, Parkinson's disease, CreutzfeldtJakob disease, normotensive hydrocephalus, etc. The aim of the study was generalization of the results of modern studies for the detailed characterization of the described model of experimental Alzheimer's dementia. Alzheimer's disease is the most common type of dementia, occurring in 50-70% of all types of dementia. Sodium azide is a colorless crystalline, highly toxic solid suitable for modeling molecular and pathomorphological Alzheimer-like symptoms in the brain of experimental animals. A thorough study of the features of modeling azide-induced dementia will allow scientists to use this model in an experiment and will allow to obtain real promising results for solving an actual scientific problem.

Tags:

Bibliography:

1. Javeed A, Dallora AL, Berglund JS, Ali A, Ali L, Anderberg P. Machine learning for dementia prediction: a systematic review and future research directions. Journal of medical systems. 2023;47(1):17.
2. Orzheshkovskyi VV, Nevmerzhytska NM. Dementsii (ohliad literatury). Chastyna 1. Neirodeheneratyvni ta sudynni dementsii. Liky Ukrainy. 2011;4(150):55-59. [in Ukrainian].
3. Orzheshkovskyi VV, Nevmerzhytska NM. Dementsii (ohliad literatury). Chastyna 2. Deiaki inshi formy dementsii. Likuvannia dementsii. Liky Ukrainy. 2011;5(151):59-60. [in Ukrainian].
4. Mayer G, Frohnhofen H, Jokisch M, Hermann DM, Gronewold J. Associations of sleep disorders with all-cause MCI/dementia and different types of dementia - clinical evidence, potential pathomechanisms and treatment options: A narrative review. Front Neurosci. 2024;18:1372326. DOI: 10.3389/fnins.2024.1372326.
5. Singla RK, Dhonchak K, Sodhi RK, Arockia Babu M, Madan J, Madaan R, et al. Bergenin ameliorates cognitive deficits and neuropathological alterations in sodium azide-induced experimental dementia. Front Pharmacol. 2022;13:994018. DOI: 10.3389/fphar.2022.994018.
6. Korde DS, Humpel C. A Combination of Heavy Metals and Intracellular Pathway Modulators Induces Alzheimer Disease-like Pathologies in Organotypic Brain Slices. Biomolecules. 2024;14(2):165. DOI: 10.3390/biom14020165.
7. Knopman DS, Lundt ES, Therneau TM, Albertson SM, Gunter JL, Senjem ML, et al. Association of Initial β-Amyloid Levels With Subsequent Flortaucipir Positron Emission Tomography Changes in Persons Without Cognitive Impairment. JAMA Neurol. 2021;78(2):217-228. DOI: 10.1001/jamaneurol.2020.3921.
8. Liessem-Schmitz A, Teske N, Scheld M, Nyamoya S, Zendedel A, Beyer C, et al. Nrf2 Signaling in Sodium Azide-Treated Oligodendrocytes Restores Mitochondrial Functions. J Mol Neurosci. 2018;66(2):229-237. DOI: 10.1007/s12031-018-1159-2.
9. Zhang RY, Zhang X, Zhang L, Wu YC, Sun XJ, Li L. Tetrahydroxystilbene glucoside protects against sodium azide-induced mitochondrial dysfunction in human neuroblastoma cells. Chin Herb Med. 2021;13(2):255-260. DOI: 10.1016/j.chmed.2020.11.007.
10. Nöldner M. Oral treatment with the Ginkgo biloba extract EGb 761® prevents sodium azide-induced memory deficits in rats. Planta Medica International Open. 2017;4:134-135.
11. Jabeen K, Rehman K, Awan FR, Aslam B, Qureshi AS. Comparative Biochemical Profiling of Aluminum Chloride and Sodium Azide Induced Neuroinflammation and Cardiometabolic Disturbance. ACS Omega. 2022;7(44):40432-40445. DOI: 10.1021/acsomega.2c05467.
12. Singla RK, Dhonchak K, Sodhi RK, Arockia Babu M, Madan J, Madaan R, et al. Bergenin ameliorates cognitive deficits and neuropathological alterations in sodium azide-induced experimental dementia. Front Pharmacol. 2022;13:994018. DOI: 10.3389/fphar.2022.994018.
13. Zhang RY, Zhang L, Zhang L, Wang YL, Li L. Anti-amyloidgenic and neurotrophic effects of tetrahydroxystilbene glucoside on a chronic mitochondrial dysfunction rat model induced by sodium azide. J Nat Med. 2018;72(3):596-606. DOI: 10.1007/s11418-018-1177-y.
14. Bell EL, Klimova T, Chandel NS. Targeting the mitochondria for cancer therapy: regulation of hypoxia-inducible factor by mitochondria. Antioxid Redox Signal. 2008;10(3):635-640. DOI: 10.1089/ars.2007.1655.
15. Yang J, Liu X, Bhalla K, Kim CN, Ibrado AM, Cai J, et al. Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked. Science. 1997;275(5303):1129-1132. DOI: 10.1126/science.275.5303.1129.
16. Yang E, Korsmeyer SJ. Molecular thanatopsis: a discourse on the BCL2 family and cell death. Blood. 1996;88(2):386-401.

Publication of the article:

«Bulletin of problems biology and medicine», 2024 Issue 2, 173, addition, 69-70 pages, index UDC 616.892.3:57.085(048.8)

DOI:

10.29254/2523-4110-2024-2-173/addition-69-70