Mounting evidence demonstrate AD-related retinal pathology in AD patients and animal models. Recent studies documented parallels between the brain and retinal pathology found both in AD patients and animal models (Koronyo-Hamaoui et al., 2011; Koronyo et al., 2012; Shi et al., 2014; Hart et al., 2016; Doustar et al., 2017; Koronyo et al., 2017; Koronyo-Hamaoui et al., 2020). While early examinations of postmortem eyes isolated from AD patients revealed loss of optic nerve integrity and RGC degeneration (Hinton et al., 1986; Blanks et al., 1989; Sadun and Bassi, 1990; Blanks et al., 1996a, b), it was not until 2010 that Koronyo-Hamaoui and colleagues were able to identify the existence of pathological hallmarks, Aβ deposits, in retinas isolated from these patients (Koronyo-Hamaoui et al., 2011). These findings were also true for MCI and other early-stage AD cases. Subsequent studies confirmed the original results and further identified pTau, characterized retinal plaque subtypes, as well as demonstrated neuronal degeneration and elevated levels of Aβ alloforms, astrogliosis and microgliosis (Alexandrov et al., 2011; Koronyo-Hamaoui et al., 2011; Koronyo et al., 2012, 2017; Schön et al., 2012; Tsai et al., 2014; Hart et al., 2016; La Morgia et al., 2016; den Haan et al., 2018; Hampel et al., 2018; Grimaldi et al., 2019; Schultz et al., 2020; Shi et al., 2020). In this review, we describe key pathological processes that were found in the AD retina (illustrated in Figure 1), with a focus on characteristic Aβ and tau accumulation and emerging retinal amyloid imaging modalities, which provide promise for advancing noninvasive methods for early disease diagnosis and monitoring.