Neuroprotection against glaucoma remains a concept
Neuroprotection against glaucoma remains a concept
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DOI：
10.1007/s00347-004-1129-7
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发表时间：
2004-11-01
期刊：
影响因子：
--
通讯作者：
Schmidt, KG
中科院分区：
文献类型：
--
作者：
Osborne, NN;Schmidt, KG
根据世卫组织的估计，全世界约有1.05亿人受青光眼影响。这可以被定义为进行性视神经病变，伴有视神经乳头的结构损伤和视网膜神经节细胞的死亡。虽然眼压升高被认为是青光眼的原因，但降低眼压通常不会导致改善。出于这个原因，其他病因的假设，这是在下面的贡献。神经保护剂在青光眼治疗中的作用进行了讨论。青光眼特有的神经节细胞死亡模式似乎表明某些神经节细胞可能比其他细胞更敏感。在这种情况下，“累积损伤”理论包括这样的假设，即许多神经再生疾病如青光眼、阿尔茨海默病或帕金森病的延迟发作可以归因于与年龄相关的神经节细胞中有毒物质的积累。相反，“单一损伤”理论是基于这样的假设，即某些神经节细胞处于由所谓的突变反应基因的表达引起的稳态降低的状态。治疗方法值得考虑的基础上，他们的副作用和疗效的动物试验。
According to estimates made by WHO, approximately 105 million people are affected worldwide by glaucoma. This can be defined as progressive optic neuropathy with structural damage of the optic nerve head and death of retinal ganglion cells. Although elevated IOP is considered responsible for glaucoma, lowering the pressure often does not result in improvement. For this reason, other etiological factors are presumed, which are presented in the following contribution. The role of neuroprotective agents in the treatment of glaucoma is discussed. The pattern of ganglion cell death specific to glaucoma seems to suggest that certain ganglion cells could be more sensitive than others. The theory of "cumulative damage" in this case includes the hypothesis that the delayed onset of many neuroclegenerative diseases such as glaucoma, Alzheimer's disease, or Parkinson's disease can be attributed to the age-related accumulation of toxic substances in the ganglion cells. On the contrary, the theory of "singular damage" is based on the assumption that certain ganglion cells are in a state of reduced homeostasis caused by the expression of so-called mutant response genes. Therapeutic approaches worthy of consideration based on their side effect profile and efficacy in animal trials, are presented.