Abstract: The prevalence of glaucoma, the second leading cause of global blindness, is increasing due to aging populations. In glaucoma, degeneration of the optic nerve and retinal ganglion cells (RGCs) causes visual field defects and eventual blindness. Elevated intraocular pressure (IOP) stands out as the best-known factor affecting glaucoma. However, there exists a subtype of glaucoma, known as normal tension glaucoma, that is not associated with high IOP. A recent study has identified various factors involved in glaucoma pathogenesis, including altered retinal blood flow, glutamate neurotoxicity, oxidative stress, and others (Shinozaki et al., 2024). Furthermore, glaucoma patients may exhibit reduced amounts of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF) or ciliary neurotrophic factor compared with age-matched controls. Studies indicate that intraocular injections of BDNF can rescue RGCs in a mouse model of optic nerve crush (ONC) through activation of its high-affinity receptor Tropomyosin receptor kinase B (TrkB). However, the transient nature of ligand-dependent activation poses limitations on the efficacy of this treatment. We have developed several systems, described in the following sections, to address and overcome these limitations.