Studies of brain samples from living patients with AD also revealed signatures specific to early stage-disease, including an increased ratio of excitatory to inhibitory activity in the parietal cortex and temporal cortex, increased expression of TGF-β pathway components important for Aβ clearance in microglia, and upregulation of amyloidogenic genes in oligodendrocytes and excitatory neurons [257]. The gene discussed is TGFB1; the disease is Alzheimer disease.