To determine whether enhancing SELENOK-mediated GluA2 palmitoylation and AMPAR assembly could alleviate cognitive and synaptic deficits in AD, we used a neuron-specific adeno-associated virus (AAV2/B10) to overexpress SELENOK (AD-OE) in 4-month-old 5 × FAD mice through retro-orbital injection, selectively targeting hippocampal neurons (Fig. 7a). This evidence concerns the gene SELENOK and Alzheimer disease.