APP and Alzheimer disease: A recent study in AD mouse models showed that there are specific sites in tau that are phospshorylated by p38γ and that while p38γ phosphorylation of tau at the post-synaptic terminal diminished the neurotoxicity of amyloid beta aggregates and rescued synaptic alterations, reduction in p38γ considerably worsened the phenotype of APP Tg mice (Ittner et al., 2016).