## 3 Current Applications
### Glaucoma  
Glaucoma represents a neurodegenerative disorder characterized by the progressive degeneration of the optic nerve head and retinal nerve fiber layer functionality [76]. The pivotal determinants of glaucoma encompass age, ischemia, and structural factors. Aging, marked by cellular senescence and functional cell deterioration, precipitates an augmented incidence of glaucoma [77]. Concurrently, structural factors, chiefly influenced by heightened intraocular pressure (IOP), delineated as the ratio of discharged aqueous humor to that produced by the ciliary body, yield substantial influence. Nonetheless, glaucoma can manifest even within the statistically normal IOP range (10-21 mmHg), named as normal-tension glaucoma (NTG). It has been demonstrated that mitochondrial dysfunction is the primary cause of optic neuropathies such as Leber's optic neuropathy, dominant optic atrophy, and some cases of glaucoma. It has also been observed that retinal ganglion cells can initiate rapid degradation of damaged mitochondria in response to acute mitochondrial damage and activate swift mitochondrial regeneration. This process is triggered by the AMPK-PGC1\(\alpha\) biogenesis axis, which is, in turn, inhibited by TBK1 [78]. [PERSON] and co-authors empirically demonstrated the adverse effects of blue light on the mitochondria of retinal ganglion cells. Furthermore, it has been postulated that blue light inflicts damage upon mitochondrial electron transport chain-related enzymes, specifically flavin and cytochrome C oxidase (CCO), instigating the generation of photochemical effects and ROS [79]. While ROS regulation is typically governed by antioxidants, eyes deformed by ischemia or myopia undergo an excessive production of ROS and mitochondrial DNA damage due to prolonged blue light exposure. This intricate cascade culminates in the loss of the visual field through a sequence of events leading to cellular demise [80]. Various studies substantiate that blue light activation induces both apoptosis and apoptotic necrosis in retinal cells, potentially underpinning the onset or exacerbation of glaucoma [81; 82; 83; 84]. The beneficial role of red light is centered on the activity of CCO, which reduces one molecule of oxygen to form two water molecules, stimulating ATP production through the proton gradient. In eyes damaged by myopia or ischemia, there is a decrease in oxygen concentration and an increase in nitric oxide concentration, which has a higher affinity for CCO, inhibiting its activity and consequently ATP production. Red light enhances the activity of CCO by photodissociating nitric oxide from CCO [78]. Some studies demonstrated the efficacy of PBM therapy in the treatment of glaucoma. It is observed that PBM has both a hypotensive and neuroprotective effect [85]. A study conducted on 20 glaucomatous patients divided into two groups demonstrated a significant reduction in IOP in the group treated with \"Thera-Red\" PBM therapy, while the placebo group did not show a significant reduction in IOP [86]. Although we cannot rely on the clinical evidence from a single case report, it is interesting to note that a patient with geographic atrophy associated with a neurodegenerative disease, treated with non-invasive PBM therapy not directly applied to ocular tissues, showed neurological improvements and positive ocular effects, including a reduction in intraocular pressure (IOP) [87]. In a murine model with induced acute glaucoma attack, PBM therapy demonstrated protective effects on ganglion cells, with significantly higher cell count compared to the untreated model and less reduction in ganglion cell layer thickness [88].