Beyond intraocular pressure: Neuroprotective strategies for future glaucoma therapy

被引:25
作者
Hartwick, ATE [1 ]
机构
[1] Univ Waterloo, Sch Optometry, Waterloo, ON N2L 3G1, Canada
关键词
neuroprotection; glaucoma; excitotoxicity; glutamate; neurotrophins; nitric oxide; calcium channel blockers;
D O I
10.1097/00006324-200102000-00008
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Background. All currently approved glaucoma medications are directed toward lowering intraocular pressure. However, it is apparent that there are pressure-independent mechanisms associated with the development of glaucomatous optic neuropathy. There has been considerable effort to develop therapeutics that rescue the retinal ganglion cells from undergoing secondary degeneration after the original insult has occurred. This therapeutic strategy has been termed neuroprotection. Methods. The literature was reviewed to examine the current knowledge of the degenerative cascade involved in glaucomatous damage, with emphasis on potential therapeutic targets for neuroprotective strategies. Results. There are a number of promising areas of research for new glaucoma therapies including glutamate antagonists, calcium channel blockers, antioxidants, nitric oxide synthase inhibitors, neurotrophins, and anti-apoptotic agents. Conclusions. Glaucoma is a complex disease with a number of risk factors and mechanisms leading to ganglion cell death. Future glaucoma therapy will likely include neuroprotectants that could be used as an adjunct therapy with other medications designed to lessen the initial insult (i.e., intraocular pressure-lowering compounds). As the word neuroprotection becomes more popular, care must be taken in evaluating the research literature for clinically effective therapies.
引用
收藏
页码:85 / 94
页数:10
相关论文
共 118 条
[111]  
Vorwerk CK, 1996, INVEST OPHTH VIS SCI, V37, P1618
[112]  
Weinreb RN, 1999, ARCH OPHTHALMOL-CHIC, V117, P1540
[113]   RISK-FACTORS FOR RATE OF PROGRESSION OF GLAUCOMATOUS VISUAL-FIELD LOSS - A COMPUTER-BASED ANALYSIS [J].
WILSON, R ;
WALKER, AM ;
DUEKER, DK ;
CRICK, RP .
ARCHIVES OF OPHTHALMOLOGY, 1982, 100 (05) :737-741
[114]   COMPARISON OF GANGLION-CELL LOSS AND CONE LOSS IN EXPERIMENTAL GLAUCOMA [J].
WYGNANSKI, T ;
DESATNIK, H ;
QUIGLEY, HA ;
GLOVINSKY, Y .
AMERICAN JOURNAL OF OPHTHALMOLOGY, 1995, 120 (02) :184-189
[115]  
Yoles E, 1999, INVEST OPHTH VIS SCI, V40, P65
[116]   Potential neuroprotective therapy for glaucomatous optic neuropathy [J].
Yoles, E ;
Schwartz, M .
SURVEY OF OPHTHALMOLOGY, 1998, 42 (04) :367-372
[117]   Elevation of intraocular glutamate levels in rats with partial lesion of the optic nerve [J].
Yoles, E ;
Schwartz, M .
ARCHIVES OF OPHTHALMOLOGY, 1998, 116 (07) :906-910
[118]   Nitrate therapy may retard glaucomatous optic neuropathy, perhaps through modulation of glutamate receptors [J].
Zurakowski, D ;
Vorwerk, CK ;
Gorla, M ;
Kanellopoulos, AJ ;
Chaturvedi, N ;
Grosskreutz, CL ;
Lipton, SA ;
Dreyer, EB .
VISION RESEARCH, 1998, 38 (10) :1489-1494