5xFAD mice present an aggressive model of amyloidosis, with several familial AD mutations that result in the overexpression of Aβ42. Studies in this model have demonstrated the presence of Aβ42 in ocular tissues including the retina as well as increases in Aβ40 in the RPE (Park et al., 2014; Parthasarathy et al., 2015; Hadoux et al., 2019). In the sporadic O. degus model of AD, Aβ deposition appears to be progressive, accumulating first in the GCL, NFL, INL and photoreceptors (Chang et al., 2020). Whole retinal histological examination via Aβ-specific staining revealed the most plaque burden in the central retina (Inestrosa et al., 2005; Du et al., 2015).