Abstract: In glaucoma, a leading cause of blindness, retinal ganglion cells are progressively damaged. Intraocular pressure reduction is the only established treatment for glaucoma (Collaborative Normal-Tension Glaucoma Study Group, 1998; Vass et al., 2007). However, in some cases, visual field loss progresses despite sufficiently reduced intraocular pressure (Collaborative Normal-Tension Glaucoma Study Group, 1998; Killer and Pircher, 2018). While intraocular pressure and age are known risk factors for glaucoma (Ernest et al., 2013), the underlying mechanisms of glaucoma progression are not fully understood. Many factors that may influence glaucoma progression, including myopia and blood flow impairment, have been investigated (Marcus et al., 2011; Ernest et al., 2013). A factor that may be related to glaucoma is the concurrent occurrence of Alzheimer’s disease, which is caused by the accumulation of amyloid β (Aβ) in the brain. Glaucomatous retinal changes in patients with Alzheimer’s disease have been reported (Wang and Mao, 2021). Other studies have reported Aβ accumulation in animal models of glaucoma with ocular hypertension (Guo et al., 2007; Ito et al., 2012). Moreover, Aβ induces apoptotic retinal ganglion cell death (Guo et al., 2007). Considering that Aβ induces retinal ganglion cell death, reducing Aβ accumulation and consequently preventing retinal ganglion cell death may be a therapeutic strategy for glaucoma (Figure 1A).