In agreement with the above findings in patients, the pathological hallmarks of AD were also described in numerous animal models of AD (see a summary in Table 1). Both the soluble and insoluble forms of Aβ were found in the retina of sporadic models and transgenic mice harboring familial AD (FAD) mutations (Ning et al., 2008; Dutescu et al., 2009; Liu et al., 2009; Perez et al., 2009; Koronyo-Hamaoui et al., 2011; Koronyo et al., 2012; Tsai et al., 2014; Du et al., 2015; Gupta et al., 2016; Hart et al., 2016; Habiba et al., 2020). Intriguingly, early manifestations of retinal Aβ plaques have also been detected prior to their occurrence in the brain (Koronyo-Hamaoui et al., 2011). Moreover, upon assessment of therapeutic response, researchers found that positive effects of immunotherapy on cerebral Aβ-plaque reduction were also reflected in the respective retinas in transgenic animal models of AD (ADtg) (Liu et al., 2009; Koronyo-Hamaoui et al., 2011; Koronyo et al., 2012; Yang et al., 2013; He et al., 2014; Gao et al., 2015; Parthasarathy et al., 2015). These studies illustrate the common retino-cerebral mechanisms of neuroprotection in response to therapy, which encourages the use of retinal imaging to noninvasively assess therapeutic efficacy in real time.