Alzheimer’s hallmark pathologies Aβ deposits and tauopathy are found in retinal cell types and topographical regions shown to undergo degeneration and physiological abnormalities in both patients and transgenic animal models (Koronyo-Hamaoui et al., 2011; Schön et al., 2012; La Morgia et al., 2016; Koronyo et al., 2017; den Haan et al., 2018; Asanad et al., 2019b; Grimaldi et al., 2019; Habiba et al., 2020; Shi et al., 2020). These findings provide a link between AD-related retinal neuropathology and the visual deficits reported in living patients. For instance, histological examination of retinal tissue shows colocalization of pTau and Aβ pathology in regions associated with RGC loss (Schön et al., 2012; La Morgia et al., 2016; Koronyo et al., 2017; den Haan et al., 2018; Asanad et al., 2019b; Grimaldi et al., 2019; Shi et al., 2020). Specifically, degeneration of RGCs would undoubtedly compromise their essential role in receiving sensory input from photoreceptors via bipolar cells, and in early stages of visual information processing and conveyance to the brain (Demb and Singer, 2015). In support of this, a recent study utilizing OCT and pattern electroretinography (ERG) in AD patients showed a linear relationship between NFL thickness and the bioelectrical integrity of RGCs and their nerve fibers, which are essential for afferent signal transduction (Ngoo et al., 2019).