MARK4 and early-onset autosomal dominant Alzheimer disease: They are also in agreement with a previous study that demonstrated that the NUAK Family Kinase 1 exclusively phosphorylated Ser356, and its ablation reduced NFT formation and rescued memory deficits and synaptic plasticity in PS19 mice.51 Interestingly, both MARK4 and NUAK Family Kinase 1 ubiquitination appears to be controlled by the ubiquitin-specific protease-9,56 and they are both associated with Alzheimer’s disease.22,23,51