We first characterized the ADNC and reactive gliosis of CTRL and AD donors via quantitative immunohistochemistry for Aβ, pTau (PHF1, pTauSer396/404), reactive astrocytes (GFAP), and reactive microglia (CD68), and also measured the cortical thickness in the temporal association neocortex. The gene discussed is GFAP; the disease is Alzheimer disease.