Regarding AD, there is a growing body of literature endorsing the concept that the two hallmarks classically discernable in the brains of affected patients and preclinical animal models—i.e., the deposits of Aβ and hyperphosphorylated tau protein—are also present in their eyes, sometimes even before the appearance of clinical cognitive symptoms, in close association with other ocular pathophysiological alterations such as nerve fiber layer thinning, the degeneration of retinal ganglion cells, vascular alterations, local inflammatory responses and gliosis [247,248,249,250,251,252]. This evidence concerns the gene MAPT and Alzheimer disease.