Статины: потенциал в лечении болезни альцгеймера. Статиндер: Альцгеймер ауруын емдеудегі потенциал
Ключевые слова:
амилоид, статины, холестерин, гематоэнцефалический барьер, гематоэнцефаликалық тосқауыл, Альцгеймер ауруы,Аннотация
Болезнь Альцгеймера (БА) является широко распространённым хроническим нейродегенеративным заболеванием, поражающим людей в возрасте 65 лет и старше, против которого до сих пор не разработано эффективных методов лечения. Данные эпидемиологических исследований свидетельствуют о том, что долговременное применение гиполиподемических препаратов статинов снижает риск развития болезни Альцгеймера. Альцгеймер ауруы 65 жастан асқан адамдарда кездесетін, әлі күнге дейін нәтижелі емдеу әдісі табылмаған, кең таралған созылмалы нейродегенеративті ауру болып табылады. Эпидемиологиялық зерттеулердің деректері ұзақ уақыт гиполиподелемикалық препараттар – статиндерді пайдалану Альцгеймер ауруының даму қаупін азайтатынын көрсетеді.Библиографические ссылки
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22 Gitter B.D., Cox L.M., Rydel R.E., May P.C. Amyloid beta peptide potentiates cytokine secretion by interleukin-1 beta-activated human astrocytoma cells // Proceedings of the National Academy of Sciences of the United States of America. –1995. –Vol. 92, № 23. – P. 10738-10741.
23 Busciglio J., Lorenzo A., Yeh J., Yankner B.A. beta-amyloid fibrils induce tau phosphorylation and loss of microtubule binding // Neuron. –1995. –Vol. 14, № 4. – P. 879-888.
24 Yan S.D., Chen X., Fu J., Chen M., Zhu H., Roher A., Slattery T., Zhao L., Nagashima M., Morser J., Migheli A., Nawroth P., Stern D., Schmidt A.M. RAGE and amyloid-beta peptide neurotoxicity in Alzheimer’s disease // Nature. –1996. –Vol. 382, № 6593. – P. 685-691.
25 Askarova S., Yang X., Sheng W., Sun G.Y., Lee J.C. Role of Abeta-receptor for advanced glycation endproducts interaction in oxidative stress and cytosolic phospholipase A(2) activation in astrocytes and cerebral endothelial cells // Neuroscience. –2011. –Vol. 199. – P. 375 385.
2 Ward A., Tardiff S., Dye C., Arrighi H.M. Rate of conversion from prodromal Alzheimer’s disease to Alzheimer’s dementia: a systematic review of the literature // Dement Geriatr Cogn Dis Extra. – 2013. – Vol. 3, № 1. – P. 320-332.
3 Tillement J.P., Papadopoulos V. Subcellular Injuries in Alzheimer’s Disease // CNS Neurol Disord Drug Targets. –2013.
4 Walsh D.M., Selkoe D.J. Aβ Oligomers – a decade of discovery // Journal of Neurochemistry. – 2007. – Vol. 101. – № 5. – P. 1172-1184.
5 Dahlgren K.N., Manelli A.M., Stine W.B., Baker L.K., Krafft G.A., LaDu M.J. Oligomeric and Fibrillar Species of AmyloidÎ ² Peptides Differentially Affect Neuronal Viability // Journal of Biological Chemistry. – 2002. – Vol. 277, № 35. – P. 32046- 32053.
6 Nistor M., Don M., Parekh M., Sarsoza F., Goodus M., Lopez G.E., Kawas C., Leverenz J., Doran E., Lott I.T., Hill M., Head E. Alpha- and beta-secretase activity as a function of age and beta-amyloid in Down syndrome and normal brain // Neurobiol Aging. – 2007. – Vol. 28, № 10. – P. 1493-1506.
7 Hardy J., Selkoe D.J. The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics // Science. –2002. –Vol. 297, № 5580. – P. 353-356.
8 Zheng W.H., Bastianetto S., Mennicken F., Ma W., Kar S. Amyloid beta peptide induces tau phosphorylation and loss of cholinergic neurons in rat primary septal cultures // Neuroscience. – 2002. – Vol. 115, № 1. – P. 201-211.
9 LaFerla F.M., Green K.N., Oddo S. Intracellular amyloid-beta in Alzheimer’s disease // Nat Rev Neurosci. – 2007. – Vol. 8, № 7. – P. 499-509.
10 Westmark C.J. What’s hAPPening at synapses? The role of amyloid beta-protein precursor and beta-amyloid in neurological disorders // Mol Psychiatry. – 2012.
11 Priller C., Bauer T., Mitteregger G., Krebs B., Kretzschmar H.A., Herms J. Synapse formation and function is modulated by the amyloid precursor protein // J Neurosci. – 2006. – Vol. 26. – № 27. – P. 7212-7221.
12 William C.M., Andermann M.L., Goldey G.J., Roumis D.K., Reid R.C., Shatz C.J., Albers M.W., Frosch M.P., Hyman B.T. Synaptic plasticity defect following visual deprivation in Alzheimer’s disease model transgenic mice // J Neurosci. – 2012. – Vol. 32, № 23. – P. 8004-8011.
13 Cole S.L., Vassar R. The Alzheimer’s disease beta-secretase enzyme, BACE1 // Molecular neurodegeneration. – 2007. – Vol. 2. – P. 22.
14 Head E., Lott I.T. Down syndrome and beta-amyloid deposition // Curr Opin Neurol. – 2004. – Vol. 17. – № 2. – P. 95-100.
15 Igbavboa U., Sun G.Y., Weisman G.A., He Y., Wood W.G. Amyloid beta-protein stimulates trafficking of cholesterol and caveolin-1 from the plasma membrane to the Golgi complex in mouse primary astrocytes // Neuroscience. – 2009. – Vol. 162. – № 2. – P. 328-338.
16 Soscia S.J., Kirby J.E., Washicosky K.J., Tucker S.M., Ingelsson M., Hyman B., Burton M.A., Goldstein L.E., Duong S., Tanzi R.E., Moir R.D. The Alzheimer’s disease-associated amyloid beta-protein is an antimicrobial peptide // PLoS One. – 2010. – Vol. 5, № 3. – P. 9505.
17 Mattson M.P., Cheng B., Davis D., Bryant K., Lieberburg I., Rydel R.E. beta-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity // J Neurosci. – 1992. – Vol. 12. – № 2. – P. 376-389.
18 Rogers J., Cooper N.R., Webster S., Schultz J., McGeer P.L., Styren S.D., Civin W.H., Brachova L., Bradt B., Ward P., et al. Complement activation by beta-amyloid in Alzheimer disease // Proceedings of the National Academy of Sciences of the United States of America. – 1992. – Vol. 89, № 21. – P. 10016-10020.
19 Arispe N., Rojas E., Pollard H.B. Alzheimer disease amyloid beta protein forms calcium channels in bilayer membranes: blockade by tromethamine and aluminum // Proc Natl Acad Sci U S A. – 1993. – Vol. 90. – № 2. – P. 567-571.
20 Behl C., Davis J.B., Lesley R., Schubert D. Hydrogen peroxide mediates amyloid beta protein toxicity // Cell. – 1994. – Vol. 77. – № 6. – P. 817-827.
21 Yang X., Askarova S., Sheng W., Chen J.K., Sun A.Y., Sun G.Y., Yao
G., Lee J.C. Low energy laser light (632.8 nm) suppresses amyloid-beta peptide-induced oxidative and inflammatory responses in astrocytes // Neuroscience. –2010. –Vol. 171, № 3. – P. 859-868.
22 Gitter B.D., Cox L.M., Rydel R.E., May P.C. Amyloid beta peptide potentiates cytokine secretion by interleukin-1 beta-activated human astrocytoma cells // Proceedings of the National Academy of Sciences of the United States of America. –1995. –Vol. 92, № 23. – P. 10738-10741.
23 Busciglio J., Lorenzo A., Yeh J., Yankner B.A. beta-amyloid fibrils induce tau phosphorylation and loss of microtubule binding // Neuron. –1995. –Vol. 14, № 4. – P. 879-888.
24 Yan S.D., Chen X., Fu J., Chen M., Zhu H., Roher A., Slattery T., Zhao L., Nagashima M., Morser J., Migheli A., Nawroth P., Stern D., Schmidt A.M. RAGE and amyloid-beta peptide neurotoxicity in Alzheimer’s disease // Nature. –1996. –Vol. 382, № 6593. – P. 685-691.
25 Askarova S., Yang X., Sheng W., Sun G.Y., Lee J.C. Role of Abeta-receptor for advanced glycation endproducts interaction in oxidative stress and cytosolic phospholipase A(2) activation in astrocytes and cerebral endothelial cells // Neuroscience. –2011. –Vol. 199. – P. 375 385.
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Как цитировать
Askarova, S., Adambekov, S., Tsoy, A., Isayeva, R. B., & Shalakhmetova, T. M. (2015). Статины: потенциал в лечении болезни альцгеймера. Статиндер: Альцгеймер ауруын емдеудегі потенциал. Вестник КазНУ. Серия биологическая, 61(2), 135–143. извлечено от https://bb.kaznu.kz/index.php/biology/article/view/192
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ФИЗИОЛОГИЯ ЧЕЛОВЕКА И ЖИВОТНЫХ, БИОФИЗИКА