Here, we show that genetic reduction of the translational repressors, Fragile X messenger ribonucleoprotein (FMRP) or eukaryotic initiation factor 4E (eIF4E)‐binding protein 2 (4E‐BP2), prevented the attenuation of hippocampal protein synthesis and memory impairment induced by AD‐linked amyloid‐β oligomers (AβOs) in mice. This evidence concerns the gene FMR1 and Alzheimer disease.