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Alpha-Lipoic Acid in Glaucoma: A Neurovascular Antioxidant StrategyGlaucoma is a progressive optic neuropathy in which elevated intraocular pressure, vascular insufficiency, and oxidative stress contribute to retinal ganglion cell (RGC) damage () (). In glaucoma, excessive reactive oxygen species (ROS) and impaired antioxidant defenses lead to DNA, protein, and lipid oxidation in the retina and optic nerve (). Augmenting the antioxidant system is therefore of great interest. Alpha-lipoic acid (ALA) is a potent, naturally occurring antioxidant that can modulate redox balance and support neurovascular health. It has gained attention for its effects in neurodegenerative and vascular diseases, including diabetic neuropathy and age-related disorders () (). Here we review evidence that ALA may reduce oxidative stress, improve endothelial function, and protect optic nerve structure, drawing on animal glaucoma models, human data, and insights from diabetes and aging research.Mechanisms of Alpha-Lipoic Acid as an AntioxidantAlpha-lipoic acid (ALA), also known as thioctic acid, is a short-chain sulfur-containing fatty acid synthesized in mitochondria. In its reduced form (dihydrolipoic acid), it scavenges ROS and reactive nitrogen species, repairs oxidized lipids and proteins, and regenerates endogenous antioxidants like glutathione and vitamins C/E () (). ALA is unique in being both fat- and water-soluble, allowing it to distribute widely in tissues and cellular compartments. It also serves as a cofactor in mitochondrial energy metabolism, supporting ATP production in high-demand cells like neurons. Together, these properties suggest ALA can bolster the aging retinal antioxidant defenses and mitigate glaucomatous oxidative damage () ().Notably, ALA interacts with key aging pathways. A classic study showed that age-related decline in the antioxidant regulator Nrf2 and glutathione synthesis in rat liver was reversed by ALA administration (). ALA increased nuclear Nrf2 and expression of glutathione-synthesizing enzymes in old animals, restoring redox balance (). More broadly, ALA levels decline with age, and supplementation has demonstrated benefits in models of age-related disorders (e.g. Parkinson’s and Alzheimer’s diseases) (). Thus ALA may counteract oxidative pathologies common to aging and glaucoma.Neuroprotection and Retinal Ganglion CellsAnimal models of glaucoma and optic nerve injury provide direct evidence that ALA supports RGC health. In the DBA/2J mouse (a genetic glaucoma model), dietary ALA markedly protected against glaucomatous RGC loss. Mice given ALA (either preventively or after glaucoma onset) showed more surviving RGCs and preserved axonal transport than untreated controls (). ALA diets also upregulated antioxidant gene/protein expression and reduced retinal markers of lipid peroxidation, protein nitration, and DNA oxidation (). In short, ALA slowed glaucoma progression in mice by bolstering antioxidant defenses and directly shielding RGCs (). In a rat optic nerve crush model (an acute injury that mimics aspects of glaucoma), prophylactic ALA injection increased RGC survival by 39% (versus ~28% when given after injury) (). ALA-treated rats had significantly higher counts of RGCs and upregulation of neuroprotective factors (erythropoietin receptor and neurotrophin-4/5) in the retina (). These findings underscore ALA’s neuroprotective efficacy for optic nerve injury: it promotes RGC survival and may engage endogenous repair p