transcorneal tas

# 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 ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC11831300/#:~:text=Glaucoma%20is%20one%20of%20the,and%20two%20multicentre%20studies%20have)). Presently, the only proven treatment slows damage by **lowering intraocular pressure (IOP)** ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC11831300/#:~:text=Glaucoma%20is%20one%20of%20the,and%20two%20multicentre%20studies%20have)); 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)** ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC10577855/#:~:text=diseases%2C%20with%20increased%20NTFs%20as,retinal%20ES)). 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 ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC10577855/#:~:text=diseases%2C%20with%20increased%20NTFs%20as,retinal%20ES)). 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 ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC10577855/#:~:text=Gene%20expression%20analysis%20of%20the,and%20bright%20blue%20light%20exposed)) ([pmc.ncbi.nlm.nih.gov](https://pmc.ncbi.nlm.nih.gov/articles/PMC10577855/#:~:text=A%20remarkable%20change%20was%20the,of%20TcES%20in%20inhibiting%20apoptosis)). For instance, TES can **increase Bcl-2 (an anti-apoptotic protein)** and **decrease Bax (a pro-ap

Electrical Stimulation for Glaucoma: Signal Boost or True Neurorestoration?

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