**7. β-Amyloid peptides altered clearance in loss vision in AD**

Until now, we have been discussing the altered clearance mechanisms of beta amyloid peptides in AD. However, these peptides are involved in other pathological mechanisms during the development and progression of AD. Recently, the βA42 peptide has been involved in vision loss and its presence in the retina has been proposed as an early diagnostic marker for AD [78– 80]. The presence of multiple βA42 reservoirs in the eye, especially in the retina environment, also induces different pathologies that lead to deficient vision as blindness [81, 82]. Pathologies such as age-related macular degeneration (AMD) and cataracts may contribute to the local inflammatory events involved in the formation of local deposits of lipids and beta amyloid peptide called drusens, atrophy of retinal pigment epithelium, lens degeneration, and photoreceptor cell death [82, 83]. In this section of the chapter, we will discuss the most recent findings emerging from the altered mechanisms of beta amyloid clearance in the eye.

As mentioned above, one of the principal degradation mechanism of amyloid beta peptides is the enzymatic pathway. In the brain, the principal βA-degrading enzymes are neprilysin, endothelin-converting enzyme (ECE), insulin-degrading enzyme (IDE), angiotensin-convert‐ ing enzyme (ACE), and in mitochondria the enzyme is called hPreP [84]. However, in the eye the presence of the Neprilysin specifically in the lens [82] has been described. In other words, it has been reported that autophagy could be involved in the degradation of beta amyloid peptides through the internalization in clathrin-positive endosomes. However, these mecha‐ nisms have not been totally elucidated and current research is being performed in order to probe it in the eye [85, 86]. Finally, as mentioned above, antibeta amyloid antibody therapy is a currently applicable treatment. In the eye, this therapy was designed to target the C-terminal fragment of βA42 in a mouse model of AMD resulting in a protective effect. All this mecha‐ nisms of Alzheimer pathophysiology can contribute to vision degeneration, suggesting further that therapeutics targeting Aβ proteases or induced autophagy may be applicable to avoid vision loss.
