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Excerpt:
Forecasting Glaucoma Vision Restoration: 5-, 10-, and 20-Year OutlookGlaucoma causes progressive loss of the retinal ganglion cells (RGCs) that send visual signals from the eye to the brain. Today’s treatments (medications, lasers or surgery) only lower eye pressure, which can slow vision loss but cannot restore lost nerve cells (). In fact, as one recent review notes, “controlling [eye pressure] in certain patients can be futile in slowing disease progression” (). New research is focused on three approaches: neurorescue to save or boost surviving RGCs; bioelectronic/cortical augmentation to bypass the damage; and true regeneration or replacement of damaged cells. These have very different timelines. Below, we explain what current trials and regulatory paths suggest for each category, using optimistic, base-case, and conservative scenarios.
Short-Term Outlook (Months–Years): Neurorescue and Neuroenhancement In the next few years, the emphasis will be on neuroprotection/neuroenhancement – therapies that aim to preserve or slightly improve the function of existing RGCs rather than re-grow them. Studies have identified factors (like neurotrophins or gene signals) that help damaged RGCs survive. For example, gene therapy in mice has shown dramatic RGC protection: one Harvard team used three Yamanaka reprogramming factors in mice with glaucoma, and found that injured optic nerves regenerated and vision improved (). This proof-of-concept is exciting, but still very early (in mice) and far from a human treatment.More clinically, several early human trials are underway. For instance, a Phase-1 trial used eye drops containing nerve growth factor (rhNGF) in glaucoma patients (). The drops were safe and well-tolerated, but the small trial did not show a statistically significant vision improvement over placebo (though there were hints of benefit) (). In other words, no rescue drug has cleared trials yet. Reviews agree that most neuroprotective strategies (drugs, supplements or cells) that work in animals have “resulted in approved therapy [for glaucoma] clinically” only in rare cases and that the “road to glaucoma neuroprotection remains long” (). Some patients and doctors try over-the-counter supplements (like citicoline, gingko, or nicotinamide) or systemic medications (e.g. brimonidine eye drops) hoping for an effect (), but none of these are proven to restore vision.A related idea is electrical stimulation of the optic nerve or retina. Small clinical studies have tested placing electrodes near the eye to deliver brief currents, with the goal of slowing degeneration. Encouragingly, one study of transorbital optic nerve stimulation (ONS) reported that after a course of noninvasive stimulation, about 63% of treated eyes showed no further visual-field loss over ~1 year (). In other words, most eyes’ vision stabilized after treatment. This suggests electrical neuromodulation may halt progression in some patients (). However, these were uncontrolled findings and need confirmation in larger trials. In fact, a large multicenter trial (the “VIRON” study) is now testing repetitive transorbital alternating current stimulation (rtACS) versus sham in glaucoma patients (). Early small trials hinted at modest visual field improvement from rtACS (), but the evidence is still limited. Results of the VIRON trial (expected in coming years) will be a key inflection point for this approach.Timeline (Short Term): Over the next 3–5 years we can expect more Phase 1/2 tri
