Reactive astrocytes in AD mediate neuroinflammation [48] and have been implicated indirectly in Aβ deposition [49], which results in severe changes in cellular functions such as energy metabolism [50], acetate metabolism [51], autophagic clearance of amyloid plaques [52], and more recently discovered, the urea cycle and the downstream MAOB-mediated putrescine-to-GABA pathway [17, 27]. The gene discussed is MAOB; the disease is amyloidosis.