Prior examinations of normal aged eyes demonstrated Aβ immunoreactivity in the sub-retinal pigment epithelium (RPE) (Loffler et al., 1995) as well as toxic Aβ oligomers in drusen in the macular RPE of aged and AMD patients (Johnson et al., 2002; Anderson et al., 2004; Luibl et al., 2006). As it relates to AD, an early biochemical evaluation of Aβ40 and Aβ42 alloforms in retinal tissues of patients showed their existence in the human AD retina, albeit without comparing to levels in control retinas nor assessing correlation with respective brain levels (Alexandrov et al., 2011). Importantly, a recent study corroborated these findings of amyloidogenic Aβ40 and Aβ42 alloforms in the retina of AD patients (Schultz et al., 2020). The study measured Aβ40 and Aβ42 levels in retinal and hippocampal tissues of human cohorts with neurodegenerative diseases and compared between ApoE ε4 carriers and non-carriers (Schultz et al., 2020). Results from this study showed higher levels of retinal and hippocampal Aβ40 and Aβ42 in individuals with AD-related pathological changes and ApoE ε4 carriers. Further, levels of both alloforms in the retina correlated with their counterparts in the hippocampus, as well as with NFT and Aβ plaque burden severity (Schultz et al., 2020).