Chronic, low-grade inflammation is a typical sign of Alzheimer’s neuropathology (Akiyama et al., 2000). Neuroinflammation in AD is linked with increased astrocyte and microglia reactivity and neurotoxicity, Aβ and tau seeding and propagation, as well as with microglia-mediated synaptic pruning (Cardona et al., 2006; Wyss-Coray, 2006; Stevens et al., 2007; Fuhrmann et al., 2010; Lee et al., 2010; Wyss-Coray and Rogers, 2012; Hong et al., 2016; Salter and Stevens, 2017; Ising et al., 2019; Friker et al., 2020). As in the brain, some histological studies have implicated inflammation in the retina of AD patients (Liew et al., 1994; Blanks et al., 1996a; Grimaldi et al., 2018). This is particularly interesting as the eye has historically been considered an immune privileged site (Zhou and Caspi, 2010). In 1996, Blanks and colleagues discovered increased GFAP expression in retinal astrocytes and Müller cells in the GCL of AD retina, suggesting astrogliosis occurs in the retina of these patients (Blanks et al., 1996a). More recently, detrimental astrocyte and microglial activation was observed along with Aβ plaques, tau tangles, and neurodegeneration in postmortem retinal tissues of 6 AD patients as compared with 6 control subjects (Grimaldi et al., 2019). Notably, molecular mediators of innate immunity including interleukin-1β (IL-1β), complement component 3 (C3), osteopontin, and triggering receptor expressed on myeloid cells 2 were found to be upregulated in retinal tissues of AD patients (Grimaldi et al., 2019).