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Fig. 9. NF-L (A), rhodopsin kinase (B), caspase-3 (C), PARP (D), GFAP (E), and AIF (F) proteins relative to actin in the retina in the nonischemic ischemia (control) and following ischemia/reperfusion with vehicle treatment (vehicle) or EGCG treatment (EGCG). Ischemia/reperfusion caused a significant change in the amounts of all proteins (except for AIF), and treatment with EGCG significantly counteracted this effect. Data are means with error bars indicating 7SEMs. n ¼ 6 in each case, po0.05, and po0.01.

Conclusion

This article makes a case for the use of substances such as creatine, a-lipoic acid, nicotinamide, and EGCG as adjunctive therapies in the treatment of glaucoma. It is argued that, on diagnosis of glaucoma, immediate treatment with a substance that enhances mitochondrial function will increase the survival of still functional ganglion cells. It is postulated that the process of ganglion cell death in glaucoma occurs in a number of stages, initiated by an ischemic insult to their axons. In this state, ganglion cells can still survive for many years, but they are nevertheless more susceptible to further insults. The final demise of a particular ganglion cell occurs when the cell’s energy metabolism reaches a critical point caused by additional insults. Potential additional insults include light or raised extracellular levels of glutamate, NO, or TNF-a. It is suggested that should a substance such as creatine, a-lipoic acid, nicotinamide, and

EGCG be available to ganglion cells in their susceptible stage, mitochondrial function will be potentially enhanced and in the process prolong ganglion survival. The potential advantage of daily intake of such nontoxic compounds by glaucoma patients to slow down visual loss is a theoretical one based on animal studies but one that makes sense. It is not suggested as an alternative to the use of IOP-lowering agents but rather as a form of adjunct treatment.

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