The signs of AD pathology included changes in neuronal morphology, the formation of syncytia, neuronal loss, amyloid-β and tau accumulation, expression changes in amyloid-β processing genes (PSEN1, PSEN2, BACE1), increased expression of pro-inflammatory cytokines (TNF-α, IFN-γ, IL-1β, IL-6, IL-10, IL-4, CXC3R) as well as gliosis characterized by changed astrocyte morphology, increased expression of genes involved in astrogliosis (e.g. glial fibrillary acidic protein, GFAP) and microglial activation (CD11b, CD68, HLADR) [145–148]. The gene discussed is GFAP; the disease is Alzheimer disease.