SYVN1 and Alzheimer disease: Indeed, we report that p-ELK1 levels are apparently increased in AD, whereas genetically knocking down ELK1 or pharmacologically inhibiting ELK1 phosphorylation enhances SYVN1-mediated ubiquitination and degradation of PS1, resulting in decreased Aβ generation and improved synaptic and cognitive function in AD model mice (Figs. 3–, 6).