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Excerpt:
Electrical Stimulation for Glaucoma: Signal Boost or True Neurorestoration?Glaucoma is a leading cause of irreversible vision loss (affecting >70 million people worldwide) characterized by loss of retinal ganglion cells and optic nerve damage (). Presently, the only proven treatment slows damage by lowering intraocular pressure (IOP) (); no therapy can actually restore lost vision. This has spurred interest in neurostimulation therapies to protect or even revive retinal neurons. Two main approaches are under study: transcorneal electrical stimulation (TES, via corneal electrodes) and transorbital or transcranial alternating-current stimulation (ACS, via electrodes near the eyes). We review sham-controlled studies of these methods in glaucoma, their proposed mechanisms, typical stimulation parameters, and the observed effects on vision (visual field and contrast sensitivity), plus practical issues of safety and availability.How Might Electrical Stimulation Help?Experimental work suggests several ways brief currents can boost neural survival and plasticity. One class of effects is neurotrophic upregulation: stimulation prompts the retina and optic nerve to produce growth factors that nourish neurons. For example, in animal models of optic injury, TES or ACS increases levels of neurotrophins such as brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF) and insulin-like growth factor (IGF-1) (). BDNF in particular is critical for retinal ganglion cell (RGC) survival and synaptic plasticity, so its upregulation may help “revive” dysfunctional but living cells. In one study, alternating currents applied to injured rats raised BDNF and CNTF in the eye (). Electrical stimulation also appears to trigger anti-apoptotic (anti-cell-death) signaling. Gene analyses in rodent retina after TES have shown downregulation of apoptotic factors and upregulation of cell-survival proteins () (). For instance, TES can increase Bcl-2 (an anti-apoptotic protein) and decrease Bax (a pro-apoptotic protein) in retinal cells (). In practical terms, these molecular shifts correlate with greater neuronal survival: in a glaucomatous injury model, TES-treated eyes had significantly more surviving RGCs at one month post-injury than untreated eyes, along with higher levels of anti-inflammatory IL-10 and less NF-κB activity (). In other words, electrical pulses suppress damaging inflammation and cell-death pathways, helping to preserve RGCs () ().Finally, electrical stimulation may engage cortical plasticity. Glaucoma deprives the brain of input from the damaged optic nerve, but some visual pathways remain intact (“residual vision”). By sending rhythmic currents to the eyes, rtACS may entrain brain waves (especially alpha-band oscillations) in visual cortex, potentially reactivating underused circuits. In one controlled trial, study authors noted that claimed vision gains from 10 Hz ACS were attributed to “increased neuronal synchronization and coherent oscillatory activity via entrainment of alpha frequencies” in occipital cortex (). This kind of neuromodulation-inspired idea – boosting brain connectivity with surviving inputs – is actively studied, although evidence in glaucoma patients remains indirect (). In summary, laboratory data suggest electrical stimulation could promote neuroprotection by (1) raising growth factors like BDNF, (2) blocking cell-death signals (e.g. by upregulating Bcl-2), (3) reducing inflammation, and (4) harnessing brain
