As discussed above, the retina undergoes neuropathological changes similar to the brain in AD patients. This is not surprising given the developmental, physiological, and anatomical similarities between the two tissue types, rendering them vulnerable to AD-related neuronal and functional abnormalities (Byerly and Blackshaw, 2009; London et al., 2013; Jindal, 2015). A host of visual and ocular manifestations were reported in both MCI and AD patients, particularly loss of contrast sensitivity, color discrimination deficits, difficulties with depth and motion perception, circadian rhythm irregularities, and sleep disturbances (Sadun et al., 1987; Katz and Rimmer, 1989; Trick et al., 1989; Cronin-Golomb et al., 1991; Cronin-Golomb, 1995; Lakshminarayanan et al., 1996; Cormack et al., 2000; Rizzo et al., 2000; Pache et al., 2003; Ng et al., 2007; Armstrong, 2009; Salamone et al., 2009; Chang et al., 2014; Nolan et al., 2014; Armstrong and Kergoat, 2015; Salobrar-Garcia et al., 2015; Hart et al., 2016; Javaid et al., 2016; La Morgia et al., 2016; Polo et al., 2017; Cerquera-Jaramillo et al., 2018; Colligris et al., 2018; Risacher et al., 2020). Importantly, retinal changes in AD patients such as RGC degeneration, reduced NFL thickness, and decreased blood circulation were linked to specific visual and ocular disturbances (Hinton et al., 1986; Blanks et al., 1989, 1996a, b; Parisi et al., 2001; Berisha et al., 2007; Paquet et al., 2007; Kesler et al., 2011).