In agreement with the observed distribution of retinal Aβ deposits in AD patients, reports have indicated NFL thinning and RGC degeneration in the GCL chiefly within the superior quadrants of the retina (Blanks et al., 1989, 1996b; Berisha et al., 2007; Lu et al., 2010; Liu et al., 2015; La Morgia et al., 2016; Asanad et al., 2019b; Grimaldi et al., 2019). In vivo OCT imaging of these patient retinas revealed degeneration in multiple retinal layers (La Morgia et al., 2017). Reduced macular thickness and volume, measured by OCT, was also found to correlate with cognitive impairment in AD patients (Iseri et al., 2006). The first study that evaluated melanopsin-containing retinal ganglion cells (mRGCs), photoreceptors known to drive circadian photoentrainment, in the postmortem retina of AD patients described a significant mRGC degeneration reflected in reduction of both dendritic density and cell number (La Morgia et al., 2017). Notably, dendrite loss and cell death were closely linked to Aβ pathology and were colocalized at sites of Aβ deposits (La Morgia et al., 2016).