Abstract: Our optic nerves are vulnerable to both traumatic and non-traumatic insults, rendering optic neuropathy a leading cause of permanent and irreversible visual impairment. Optic neuropathies can arise from hereditary [e.g., dominant optic atrophy (DOA) and Leber hereditary optic neuropathy (LHON)], ischaemic (e.g., anterior and posterior ischaemic optic neuropathy), inflammatory (e.g., optic neuritis), toxic (e.g., methanol, ethambutol) and nutritional (e.g., vitamin B12 deficiency), or traumatic conditions. Amongst these, glaucomatous optic neuropathy represents the most prevalent form and constitutes the second leading cause of blindness worldwide, with approximately 10% of patients developing bilateral blindness. Currently, over 76 million people are affected by glaucoma globally—a number predicted to rise to 112 million by 2040. Current treatments primarily focus on lowering intraocular pressure (IOP) through topical medications and surgical interventions. However, a recent study from the United Kingdom Glaucoma Treatment Study demonstrated that whilst IOP-lowering treatments effectively slow disease progression, they fail to reverse visual field deficits (Reddingius et al., 2025), underscoring the urgent need for novel therapeutic strategies that proactively restore visual function by directly targeting affected retinal neurons responsible for conveying visual information to the brain.