In addition, the substantial loss of PDGFRβ, especially in the ST and TI quadrants that colocalized with retinal vascular amyloidosis, and previous corroborating data indicating significant abnormalities in the ST and TI regions, imply that inner cellular layers in the central temporal hemiretina are more susceptible to AD pathological processes [6, 26, 47, 50, 82]. This evidence concerns the gene PDGFRB and Alzheimer disease.