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Excerpt:
Neuroprotection Beyond Pressure: What’s Real, What’s HypeGlaucoma causes vision loss by damaging the optic nerve, often linked to high intraocular pressure (IOP) in the eye. Lowering IOP with drops or surgery is currently the only proven way to slow glaucoma’s progression (). However, many patients still lose vision despite good pressure control, so doctors are studying pressure-independent strategies to directly protect the retinal nerve cells (neuroprotection). This article reviews the latest research on these strategies and separates solid science from overhyped claims. A recent review reminds us that after decades of work, “only a handful of neuroprotective therapies have succeeded clinically” (). In other words, very few treatments beyond pressure-lowering have demonstrated clear benefit in patients. For now, all patients should understand that the best evidence still supports aggressive pressure control, while other approaches remain experimental () ().Alpha-2 Adrenergic Agonists (Brimonidine and Similar Drugs)One class of glaucoma medication with proposed neuroprotective effects is the alpha-2 adrenergic agonists. The most common example is brimonidine, an eye drop that lowers pressure but also signals through alpha-2 receptors in the retina. In animal studies, brimonidine showed promise as a nerve protector. For example, a 2021 experiment in mice found that topical brimonidine reduced inflammatory stress and preserved retinal ganglion cell (RGC) function after injury (). In that study, electrical signals from the retina were higher and fewer nerve cells died in treated eyes.Despite these encouraging lab results, clinical trials in humans have not confirmed a clear benefit. A 2020 systematic review of all brimonidine trials found only a few small studies, showing mixed results and high uncertainty (). Another analysis concluded overall evidence is “inconclusive” (). In one randomized trial, patients on brimonidine did not significantly fade less in vision field loss compared to standard treatment, and authors cautioned that bias may account for any apparent advantage () (). In short, brimonidine remains a useful IOP-lowering drug, but its neuroprotective powers in people have yet to be proven () ().NMDA Blockade (Memantine Trials)Another idea was to use NMDA-receptor antagonists to block excitotoxicity (overstimulation by glutamate). Memantine is an Alzheimer’s drug with that action. Two large Phase-3 trials (over 2,200 patients with open-angle glaucoma) tested oral memantine (10 mg or 20 mg daily) against placebo for four years () (). Disappointingly, memantine did not slow glaucoma progression. The rate of visual field loss was essentially the same in memantine and placebo groups () (). In pooled analysis, memantine showed no significant protective effect on visual field or optic nerve damage () (). In fact, those trials “did not reveal a significant benefit” of memantine () and failed to meet their primary endpoint (). In plain terms, memantine did not work as a glaucoma neuroprotectant, so it is not used for this purpose. Rho-Kinase Pathway InhibitorsRho-kinases (ROCK) are enzymes that regulate cell shape and contraction. In the eye, ROCK inhibitors (such as ripasudil, netarsudil) are a new type of pressure-lowering drop. They make fluid drain more easily by relaxing the eye’s drainage channels. Researchers have also found Rho-kinase blockers may directly protect nerve cells. In animal studies, topical ROCK inhibitors reduced RGC death after pressure injury. For i
