GSK3B and Alzheimer disease: In a mouse model of LPS from E. coli O55:B55-induced neuroinflammation, both gene deletion and pharmacological inhibition of the calcium-activated potassium channel KCa3.1, which is active in the phenotypic switch that occurs during astrogliosis in Alzheimer’s disease and ischemic stroke decreased CNS glia inflammation, including reactive astrogliosis and microglial activation via the Akt/GSK3β signaling pathway (73).