An AD-like phenotype could also be established in mice by conditional WT GSK3β overexpression in neurons, resulting in typical AD-associated neuronal alterations and severe brain inflammation (apoptotic cells, activated microglia expressing increased levels of TNF, IL-1, IFN-γ, KC, and macrophage inflammatory proteins 1a and 3a) [174]. This evidence concerns the gene IFNG and Alzheimer disease.