Our results demonstrate that ELK1 aberrantly increases in AD and genetic or pharmacological inhibition of ELK1 can alleviate AD-related pathology and memory impairments by enhancing the SYVN1-mediated PS1 ubiquitination and degradation, indicating that ELK1 may be a novel target for AD treatment. The gene discussed is SYVN1; the disease is Alzheimer disease.