Compared to non-AD arteries, the co-localization of THY1 or PDPN with LOX (lysyl oxidase), a general FB2 marker, raised up from 6% or 5% in non-AD to 72% or 64% in AD, respectively, suggesting a significant increase of dFB2 in AD pathogenesis (Figure 5B-D). The gene discussed is THY1; the disease is Alzheimer disease.