Hypotensive glaucoma therapy and neuroprotection
https://doi.org/10.21516/2072-0076-2020-13-2-78-82
Abstract
Most modern antihypertensive drugs used in the treatment of primary open-angle glaucoma have an indirect neuroprotective effect not only because they reduce intraocular pressure (IOP), but also because of a stimulating effect on the natural metabolic processes in the eye. Researchers and clinicians today follow the strategy of compensating IOP, starting from the earliest stages of glaucomatous optic neuropathy (GON), regardless of which drug (generic or original) reduces IOP and which combination of the main active substances this drug has. The need for neuroprotective therapy in clinical practice mainly appears either in the far advanced stages or in cases of progressive loss of visual functions. However, given the multifactorial nature of GON, it is extremely important to add neuroprotective treatment in time, starting from the early stages. Electrophysiological and morphometric studies can provide objective monitoring of neuroprotective therapy. In order to increase the effectiveness of treatment, hypotensive therapy should be supplemented by early use of direct neuroprotectors targeted at oxidative stress, and excitotoxicity and affecting other molecular mechanisms of glaucoma so as the primary events of neurodegeneration could be blocked.
About the Authors
A. N. Zhuravleva
Helmholtz National Medical Research Center of Eye Diseases
Russian Federation
Russian Federation
Anastasia N. Zhuravleva — Cand. of Med. Sci., researcher of the glaucoma department
14/19, Sadovaya-Chernogryazskaya St., Moscow, 105062
M. V. Zueva
Helmholtz National Medical Research Center of Eye Diseases
Russian Federation
Russian Federation
Marina V. Zueva — Dr of Biol. Sci., Professor, head of the department of clinical physiology of vision named after S.V. Kravkov
14/19, Sadovaya-Chernogryazskaya St., Moscow, 105062
References
1. Putilina M.V. The combined use of neuroprotectors in the treatment of cerebrovascular diseases. Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova. 2016; 116 (11): 58–63 (in Russian). doi: 10.17116/jnevro201611611158-63
2. Neroev V.V., Zueva M.V., Zhuravleva A.N., Tsapenko I.V. Structural and functional disorders in glaucoma: the prospects for preclinical diagnosis. Part 2. Electrophysiological markers of early neuroplastic events. Ophthalmology in Russia. 2020, in press (in Russian).
3. Gordon M.O., Beiser J.A., Brandt J.D., et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch. Ophthalmol. 2002; 120 (6): 714–20. doi:10.1001/archopht.120.6.714
4. Jiang X., Varma R., Wu S., et al. Los Angeles Latino Eye Study Group. Baseline risk factors that predict the development of open-angle glaucoma in a population: the Los Angeles Latino Eye Study. Ophthalmology. 2012; 119 (11): 2245–53. doi: 10.1016/j.ophtha.2012.05.030
5. Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Am. J. Ophthalmol. 1998; 126 (4): 487–97.
6. Chauhan B.C., Mikelberg F.S., Artes P.H., et al. Canadian Glaucoma Study: 3. Impact of risk factors and intraocular pressure reduction on the rates of visual field change. Arch. Ophthalmol. 2010; 128 (10): 1249–55. doi: 10.1001/archophthalmol.2010.196
7. Heijl A., Leske M.C., Bengtsson B., Hyman L., Hussein M. Early Manifest Glaucoma Trial Group. Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial. Arch. Ophthalmol. 2002; 120 (10): 1268–79. doi:10.1001/archopht.120.10.1268
8. Leske M.C., Heijl A., Hyman L., Bengtsson B., Komaroff E. Factors for progression and glaucoma treatment: the Early Manifest Glaucoma Trial. Curr. Opin. Ophthalmol. 2004; 15 (2): 102–6. doi: 10.1097/00055735-20040400000008
9. Webers C.A., Beckers H.J., Nuijts R.M., Schouten J.S. Pharmacological management of primary open-angle glaucoma: second-line options and beyond. Drugs Aging. 2008; 25 (9): 729–59. doi: 10.2165/00002512-200825090-00002
10. Noecker R.S., Dirks M.S., Choplin N.T., et al. The Bimatoprost/Latanoprost Study Group. A six-month randomized clinical trial comparing the intraocular pressure-lowering efficacy of bimatoprost and latanoprost in patients with ocular hypertension or glaucoma. Am. J. Ophthalmol. 2003; 135 (1): 55–63. https://doi.org/10.1016/S0002-9394(02)01827-5
11. Parrish R.K., Palmberg P., Sheu W.P., XLT Study Group. A comparison of latanoprost, bimatoprost, and travoprost in patients with elevated intraocular pressure: a 12-week, randomized, masked-evaluator multicenter study. Am. J. Ophthalmol. 2003; 135 (5): 688–703. doi:10.1016/s0002-9394(03)00098-9
12. Marquis R.E., Whitson J.T. Management of glaucoma: focus on pharmacological therapy. Drugs Aging. 2005; 22 (1): 1–21. doi: 10.2165/00002512-200522010-00001
13. Sherwood M.B., Craven E.R., Chou C., et al. Twice-daily 0.2 % brimonidine – 0.5 % timolol fixed combination therapy vs monotherapy with timolol or brimonidine in patients with glaucoma or ocular hypertension: a 12-month randomized trial. Arch. Ophthalmol. 2006; 124 (9): 1230–8. doi: 10.1001/archopht.124.9.1230
14. Woodward D.F., Chen J. Fixed-combination and emerging glaucoma therapies. Exp. Opin. Emerg. Drugs. 2007; 12 (2): 313–27. doi: 10.1517/14728214.12.2.313
15. McKinnon S.J., Goldberg L.D., Peeples P., Walt J.G., Bramley T.J. Current management of glaucoma and the need for complete therapy. Am. J. Manag. Care. 2008; 14 (1 Suppl): 20–7.
16. Quaranta L., Biagioli E., Riva I., et al. Prostaglandin analogs and timololfixed versus unfixed combinations or monotherapy for open-angle glaucoma: a systematic review and meta-analysis. J. Ocular Pharmacol. Therap. 2013; 29 (4): 382–9. doi: 10.1089/jop.2012.0186
17. Goldberg I., Gil Pina R., Lanzagorta-Aresti A., et al. Bimatoprost 0.03 %/timolol 0.5 % preservative-free ophthalmic solution versus bimatoprost 0.03 %/timolol 0.5 % ophthalmic solution (Ganfort) for glaucoma or ocular hypertension: a 12-week randomised controlled trial. Br. J. Ophthalmol. 2014; 98 (7): 926–31. doi:10.1136/bjophthalmol-2013-304064
18. Khouri A.S., Realini T., Fechtner R.D. Use of fixed-dose combination drugs for the treatment of glaucoma. Drugs Aging. 2007; 24 (12): 1007–16. doi: 10.2165/00002512-200724120-00004
19. Konstas A.G.P., Hollo G., Mikropoulos D.G., et al. 24-hour efficacy of the bimatoprost–timolol fixed combination versus latanoprost as first choice therapy in subjects with high-pressure exfoliation syndrome and glaucoma. Br. J. Ophthalmol. 2013; 97 (7): 857–61. doi: 10.1136/bjophthalmol-2012-302843
20. García-López A., Paczka J.A., Jiménez-Román J., Hartleben C. Efficacy and tolerability of fixed-combination bimatoprost/timolol versus fixed-combination dorzolamide/brimonidine/timolol in patients with primary open-angle glaucoma or ocular hypertension: a multicenter, prospective, crossover study. BMC Ophthalmology. 2014; 14: 161. doi:10.1186/1471-2415-14-161
21. Brief G., Lammich T., Nagel E., et al. Fixed combination of bimatoprost and timolol in patients with primary open-angle glaucoma or ocular hypertension with inadequate IOP adjustment. Clinical ophthalmology (Auckland, NZ). 2010; 14: 1125-9. doi: 10.2147/OPTH.S13074
22. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. The AGIS Investigators. Am. J. Ophthalmol. 2000;130 (4): 429–40. doi: 10.1016/s0002-9394(00)00538-9
23. Kass M.A., Heuer D.K., Higginbotham E.J., et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch. Ophthalmol. 2002; 120 (6): 701–13. doi:10.1001/archopht.120.6.701
24. Lichter P.R. Expectations from clinical trials: results of the Early Manifest Glaucoma Trial. Arch. Ophthalmol. 2002; 120 (10): 1371–2. doi: 10.1001/archopht.120.10.1371
25. Susanna R.Jr., De Moraes C.G., Cioffi G.A., Ritch R. Why do people (still) go blind from glaucoma? Transl. Vis. Sci. Technol. 2015; 4 (2):1. doi:10.1167/tvst.4.2.1
26. Gupta N, Yücel Y. Glaucoma as a neurodegenerative disease. Curr. Opin. Ophthalmol. 2007; 18: 110–4. doi:10.1097/ICU.0b013e3280895aea
27. Calkins D.J., Horner P.J. The cell and molecular biology of glaucoma: axonopathy and the brain. Invest. Ophthalmol. Vis. Sci. 2012; 53 (5): 2482–4. doi: 10.1167/iovs.12-9483i
28. Lawlor M., Danesh-Meyer H., Levin L.A., et al. Glaucoma and the brain: Trans-synaptic degeneration, structural change, and implications for neuroprotection. Surv. Ophthalmol. 2018; 63 (3): 296–306. https://doi.org/10.1016/j.survophthal.2017.09.010
29. Lebrun-Julien F., Di Polo A. Molecular and cell-based approaches for neuroprotection in glaucoma. Optom. Vis. Sci. 2008; 85 (6): 417–24. doi: 10.1097/OPX.0b013e31817841f7
30. Stevens B., Allen N.J., Vazquez L.E., et al. The classical complement cascade mediates CNS synapse elimination. Cell 2007; 131 (6): 1164–78. doi: 10.1016/j.cell.2007.10.036
31. Lopez J.C. Quantifying synaptic efficacy 2002; 3 (5): 332. doi:10.1038/nrn814
32. Frishman L.J., Freeman A.W., Troy J.B., Schweitzer-Tong D.E., Enroth-Cugell C. Spatiotemporal frequency responses of cat retinal ganglion cells. J. Gen. Physiol. 1987; 89 (4): 599–628. doi: 10.1085/jgp.89.4.599
33. Porciatti V., Ventura L.M. Physiological significance of steady-state PERG losses in glaucoma: clues from simulation of abnormalities in normal subjects. J. Glaucoma. 2009; 18 (7): 535–42. doi: 10.1097/ijg.0b013e318193c2e1
34. Morgan J.E. Retina ganglion cell degeneration in glaucoma: an opportunity missed? A review. Clin. Exp. Ophthalmol. 2012; 40: 364–8. doi: 10.1111/j.14429071.2012.02789.x
35. Shou T., Liu J., Wang W., Zhou Y., Zhao K. Differential dendritic shrinkage of alpha and beta retinal ganglion cells in cats with chronic glaucoma. Invest. Ophthalmol. Vis. Sci. 2003; 44: 3005-10. https://doi.org/10.1167/iovs.02-0620
36. Porciatti V., Ventura L.M. Retinal ganglion cell functional plasticity and optic neuropathy: a comprehensive model. J. Neuroophthalmol. 2012; 32 (4): 354–8. doi: 10.1097/WNO.0b013e3182745600
37. Liu M., Duggan J., Salt T.E., Cordeiro M.F. Dendritic changes in visual pathways in glaucoma and other neurodegenerative conditions. Exp. Eye Res. 2011; 92: 244–50. https://doi.org/10.1016/j.exer.2011.01.014
38. Zueva M.V. Dynamics of retinal ganglion cell death in glaucoma and its functional markers. Natsional’nyi zhurnal glaukoma. 2016; 15 (1): 70–85 (in Russian).
39. Francardo V., Schmitz Y., Sulzer D., Cenci M.A. Neuroprotection and neurorestoration as experimental therapeutics for Parkinson's disease. Exp. Neurol. 2017; 298: 137–47. https://doi.org/10.1016/j.expneurol.2017.10.001
40. Calkins D.J. Critical pathogenic events underlying progression of neurodegeneration in glaucoma. Prog. Retin. Eye Res. 2012; 31: 702–19. doi:10.1016/j.preteyeres.2012.07.001
41. Abbott C.J., Choe T.E., Burgoyne C.F., et al. Comparison of retinal nerve fiber layer thickness in vivo and axonal transport after chronic intraocular pressure elevation in young versus older rats. PLoS One. 2014; 9 (12): e114546. doi:10.1371/journal.pone.0114546
42. Porciatti V., Nagaraju M. Head-up tilt lowers IOP and improves RGC dysfunction in glaucomatous DBA/2J mice. Exp. Eye Res. 2010; 90: 452–60. doi:10.1016/j.exer.2009.12.005
43. Pfennigsdorf S., de Jong L., Makk S., et al. A combined analysis of five observational studies evaluating the efficacy and tolerability of bimatoprost/ timolol fixed combination in patients with primary open-angle glaucoma or ocular hypertension. Clinical Ophthalmology (Auckland, NZ). 2013; 7: 1219-25. doi: 10.2147/OPTH.S41885
44. Harris A., Jonersu C., Kagemann L. Effect of dorzolamide-timolol combination versus timolol 0,5% on ocular blood flow in patients with primary open-angle glaucoma. Am. J. Ophthalmol. 2001; 132: 490–5. doi: 10.1016/S00029394(01)01158-8
45. Izzotti A., Saccà S.C. Sensitivity of ocular anterior chamber tissues o oxidative damage and its relevance to the pathogenesis of glaucoma. Invest. Ophthalmol. Vis. Sci. 2009; 50 (11): 5251–8. https://doi.org/10.1167/iovs.09-3871
46. Saccà S.C., Pascotto A., Camicione P., Capris P., Izzotti A. Oxidative DNA damage in the human trabecular meshwork: clinical correlation in patients with primary open-angle glaucoma. Arch. Ophthalmol. 2005; 123 (4): 458–63. doi:10.1001/archopht.123.4.458
47. Izzotti A., Saccà S.C., Di Marco B., Penco S., Bassi A.M. l. Antioxidant activity of timolol on endothelial cells and its relevance for glaucoma course. Eye (Lond). 2008; 22 (3): 445–53. doi: 10.1038/sj.eye.6702737
48. Miyamoto N., Izumi H., Miyamoto R., et al. Nipradilol and timolol induce Foxo3a and peroxiredoxin 2 expression and protect trabecular meshwork cells from oxidative stress. Invest. Ophthalmol. Vis. Sci. 2009; 50:2777–84. doi: 10.1167/iovs.08-3061
49. Gross R., Hensley S., Gao F., Wu S.M. Retinal ganglion cell dysfunction induced by hypoxia and glutamate: potential neuroprotective effects of beta-blockers. Surv. Ophthalmol. 1999; 43(supp1): 162–70. doi: 10.1016/s00396257(99)00054-5
50. Kurysheva N.I., Azizova O.A., Piryazev A.P. Antioxidant activity of dorzolamide/timolol fixed combination in neuroprotective therapy in glaucoma. Ophthalmology in Russia. 2012; 9 (4): 47–51. https://doi.org/10.18008/1816-5095-2012-4-47-51 (in Russian).
51. Stjernschantz J., Selen G., Astin M., Resul B. Microvascular effects of selective prostaglandin analogues in the eye with special reference to latanoprost and glaucoma treatment. Prog. Retin. Eye Res. 2000; 19: 459–96. doi: 10.1016/s1350-9462(00)00003-3
52. Lambert W.S., Ruiz L., Crish S.D., Wheeler L.A., Calkins D.J. Brimonidine prevents axonal and somatic degeneration of retinal ganglion cell neurons. Mol. Neurodegener. 2011; 6:4. doi: 10.1186/1750-1326-6-4
53. Kudo H., Nakazawa T., Shimura M., et al. Neuroprotective effect of latanoprost on rat retinal ganglion cells. Graefe's Arch. Clin. Exp. Ophthalmol. 2006; 244: 1003–9. https://doi.org/10.1007/s00417-005-0215-0
54. Nakanishi Y., Nakamura M., Mukuno H., et al. Latanoprost rescues retinal neuro-glial cells from apoptosis by inhibiting caspase-3, which is mediated by p44/p42 mitogen-activated protein kinase. Exp. Eye Res.2006; 83: 1108–17. doi: 10.1006/exer.2000.0975
55. Yamagishi R., Aihara M., Araie M. Neuroprotective effects of prostaglandin analogues on retinal ganglion cell death independent of intraocular pressure reduction. Exp. Eye Res. 2011; 93 (3): 265–70. doi: 10.1016/j.exer.2011.06.022
56. Kanamori A., Naka M., Fukuda M., Nakamura M., Negi A. Latanoprost protects rat retinal ganglion cells from apoptosis in vitro and in vivo. Exp. Eye Res. 2009; 88: 535–41. doi: 10.1016/j.exer.2008.11.012
57. Vidal L., Diaz F., Villena A., et al. Reaction of Muller cells in an experimental rat model of increased intraocular pressure following timolol, latanoprost and brimonidine. Brain Res. Bulletin. 2010; 82: 18–24. doi: 10.1016/j.brainresbull.2010.02.011
58. Emre S., Gul M., Ates B., et al. Comparison of the protective effects of prostaglandin analogues in the ischemia and reperfusion model of rabbit eyes. Exp. Anim. 2009 Oct; 58: 505–13. doi:10.1538/expanim.58.505
Review
For citations:
Zhuravleva A.N., Zueva M.V. Hypotensive glaucoma therapy and neuroprotection. Russian Ophthalmological Journal. 2020;13(2):78-82. (In Russ.) https://doi.org/10.21516/2072-0076-2020-13-2-78-82
Views:
1516
Email this article 