NEUROPROTECTION STRATEGIES IN GLAUCOMA: CURRENT EVIDENCE AND FUTURE DIRECTIONS.

Abstract

Glaucoma, a leading cause of irreversible blindness, is characterized by progressive retinal ganglion cell (RGC) death and optic nerve degeneration. While intraocular pressure (IOP) reduction remains the primary therapeutic target, a significant proportion of patients continue to experience visual field progression despite well-controlled IOP, highlighting the multifactorial nature of the disease. This abstract explores current evidence and future directions in neuroprotection strategies, which aim to directly preserve RGC viability independent of IOP lowering. Current research focuses on various mechanisms, including enhancing mitochondrial function, reducing oxidative stress, modulating inflammation, and inhibiting excitotoxicity. Preclinical studies and early-phase clinical trials have investigated agents such as nicotinamide (Vitamin B3), citicoline, brimonidine, and various antioxidants, showing promising results in protecting RGCs from glaucomatous damage. Nicotinamide, for instance, has demonstrated potential in improving RGC function and reducing neurodegeneration by boosting cellular energy metabolism. However, the translation of these findings into robust, widely adopted clinical practice remains challenging, often due to issues of systemic toxicity, delivery methods, and inconsistent clinical trial outcomes. Future directions emphasize combination therapies targeting multiple pathogenic pathways, novel drug delivery systems for sustained ocular exposure, and personalized medicine approaches based on an individual's genetic and molecular profile. Furthermore, the burgeoning fields of gene therapy and stem cell research hold immense promise for not only protecting but potentially regenerating lost RGCs, offering hope for a more comprehensive treatment paradigm for glaucoma.