Pathogenetic aspects of the drug in the treatment of glaucoma Cortexin optic neuropathy
ARTICLE PDF (Русский)

Keywords

glaucoma, apoptosis, glaucomatous optic neuropathy, free radicals, peptides, ischemia, oxidative stress, Cortexin, neuroprotection.

How to Cite

Radchenko, J. (2015). Pathogenetic aspects of the drug in the treatment of glaucoma Cortexin optic neuropathy. East European Journal of Neurology, (2(2), 36-40. https://doi.org/10.33444/2411-5797.2015.2(2).36-40

Abstract

Glaucoma is one of the first places among the causes of blindness and visual disability in the world. Currently, glaucoma is not treated as an isolated ocular pathology as well as a manifestation of the general exchange violations and neurovascular disorders in the body. The article presents the etiology and pathogenesis of glaucomatous optic neuropathy. Microcirculatory disorders observed in the form of a narrowing of the arteries and reduce the resulting perfusion pressure, the development of capillary stasis and rheological disorders (increased aggregation of red blood cells, reducing their ability to deformation). All this subsequently leads to local metabolic disorders. It is also an important role in the pathological chain may be joining vasospasm. The results of Cortexin use in various forms of glaucoma in both monotherapy and in treatment. Cortexin use in various forms of glaucoma as a monotherapy and in treatment. Cortexin peptide bioregulators, which reduces neuronal apoptosis, provides a neuroprotective and neurotrophic effects.

https://doi.org/10.33444/2411-5797.2015.2(2).36-40
ARTICLE PDF (Русский)

References

[1] Myron Yanoff, Jay S. Duker. Ophthalmology. — 3rd. — Mosby Elsevier, 2009. — P. 1096.
[2] Ling Z.H.,Sun X.H. Glial cell and glaucomatous optic neuropathy Prog Retin Res.2013;31(2):152-181.
[3] Straubhaar M.,OrgulS.,Gukleta K., Chorioida ldopler flowmetryin healthy subjects //Arch. Ophtalmol .-2000.-Vol.118-P.211-215.
[4] Курышева Н.И. «Глаукомная оптическая нейропатия »// МЕД- пресс-информ 2006г. С.25.
[5] Flammer J. Glaucoma. –Verlag Hans Huber, 2001. -416p.
[6] Oliver J.E., Hattenhauer M.G., Herman D. etal. Blindness and glaucoma: a comparison of patients progressing to blindness from glaucoma with patients maintainingvision // Am. J. Ophthalmol. 2002. № 133. Р. 764–772.
[7] Курышева Н.И. Глаукомная оптическая нейропатия М. МЕД- пресс-информ,2006. 136с.
[8] Gupta N., Yucel Y.H. Glaucoma as a neurodegenerative disease // Curr. Opin. Ophthalmol. 2007. № 2. Р. 110–114.
[9] Bayer A.U., Keller O.N., Ferrari F., Maag K.P. Association of glaucoma with neurodegenerative diseases with apoptotic cell death: Alzheimer’s disease and Parkinson’s disease // Am. J. Ophthalmol. 2002. № 1. Р. 135–137.
[10] Bizrah M., Guo L., Cordeiro M.F. Glaucoma and Alzheimer’s disease in the elderly //Aging Health. 2011. № 5. Р. 719–733.
[11] Gupta N., Ang L–C., Noel de Tilly L. et al. Human glaucoma and neural degeneration in intracranial optic nerve, lateral geniculate nucleus, and visual cortex // Br. J. Ophthalmol. 2006. № 90. Р. 674–678.
[12] Алексеев В.Н., Газизова И.Р. Нейродегенеративные изменения у больных первичной открытоугольной глаукомой // Практическая медицина. 2012.
[13] Garaci F.G., Bolacchi F., Cerulli A. et al. Optic Nerve and Optic Radiation Neurodegeneration in Patients with Glaucoma: In Vivo Analysis with 3–T Diffusion–Tensor MR Imaging // Radiol. 2009. № 2. Р. 496–501.
[14] Iba–Zizen M.T., Istoc A., Cabanis E.A. The results of MRI exploration of glaucoma patients: what are the benefits? // Fr. Ophtalmol. 2008. № 6. Р. 24–28.
[15] Goldblum D., Kipfer–Kauer A., Sarra G.M. et al. Distribution of amyloid precursor protein and amyloid–beta immunoreactivity in DBA/2J glaucomatous mouse retinas // Inves. Ophthalmol. & Vis. Sci. 2007. № 11. Р. 5085–5090.
[16] Wang W.H., McNatt L.G., Pang I.H. et al. Increased expression of serum amyloid A in glaucoma and its effect on intraocular pressure // Inves. Ophthalmol. & Vis. Sci. 2008. №5. Р. 1916–1923.
[17] Nucci C., Martucci A., Martorana A. et al. Glaucoma progression associated with altered cerebral spinal fluid levels of amyloid beta and tau proteins // Clin. &Experim. Ophthalmol. 2011. №3. Р. 279–281.
[18] Pinelis V. G. Neuroprotective effects of cortagen, cortexin and semax on glutamate neurotoxicity / V. G. Pinelis, T. P. Storozhevykh, A. M. Surin [et al.] // J. Peptide Science. — 2008. — Vol. 14, № 8, Suppl. — P. 159–160.
[19]Герасимова М. М. Влияние Кортексина на цитокиновый обмен при пояснично-крестцовых радикулопатиях / М. М. Герасимова, А. Ю. Петушков // Нейроиммунология. — 2004. — Т. II, № 2. — С. 26.
[20] Волик Е.И. Опыт применения Кортексина в терапии глаукомной оптической нейропатии // TERRA MEDICA NOVA № 2/2006 С.1-3.
[21] Щербинина И.В., Каменских Т.Г., Колбенев И.О. Эффективность комплексного лечения глаукомной оптической нейропатии препара- том «Кортексин»//Саратовский научно-медицинский журнал.2010 Т.6. №4С.775-779.
[22] Марченко Л.Н.,Рожко Ю.И.,Кривун А.О. Пептиды Ретиналамин и Кортексин в нейропротекторной терапии глаукомы//ARSMEDICA № 13(33)2010 С. 40-46.