In the current study, we provided the first in vivo and in vitro evidence that the Aβ1-42-induced abnormal increase in Ras activity may account for the impairment of NMDAR-dependent LTP induction and spatial cognition through the downregulation of Src, suggesting that targeting Ras signaling may be an effective strategy to protect hippocampal synaptic plasticity against Aβ-induced cognitive decline at early stages of AD. The gene discussed is SRC; the disease is Alzheimer disease.