摘要
近年来随着对青光眼性视神经病变机制的深入研究,已证实兴奋性氨基酸与青光眼视网膜神经节细胞凋亡密切相关。21世纪青光眼的治疗模式正从传统的单纯降眼压向降眼压的同时从其他途径进一步加强神经保护转变,基础实验及部分临床研究证实干扰兴奋性氨基酸产生神经毒性的各环节均对神经元有保护作用,由此可以推测通过对兴奋性氨基酸的研究有望实现青光眼治疗史上的重大突破。
Recent researches have suggested that excitatory amino acids (EAA) is a final common pathway for neurologic disorders.The link between EAA and apotosis of re tinal ganglion cells (RGC) of glaucoma has been widely studied and confirmed. Ne uroprotection is a potential treatment for glaucomatous optic neuropathy which m ay independently lower intraocular pressure (IOP). It has been supported by labo ratory studies or some clinical studies that interruption of each stage of this schema is neuroprotective. It may therefore be possible to get a breakthrough in the threatment of glaucoma by blocking the pathway of EAA. ·
出处
《国际眼科杂志》
CAS
2004年第4期668-674,共7页
International Eye Science
关键词
兴奋性氨基酸
青光眼
兴奋毒
谷氨酸盐
视网膜神经节细胞
glaucoma
excitatory amino acids
excitotoxicity
glutamate
N-meth yl-D-aspartate
retinal ganglion cells
neuroprotection
