Attenuation of translational repression rescues memory impairment in Alzheimer`s disease mice

Alzheimer’s disease (AD) is characterized by impaired synaptic plasticity and progressive memory deficits. Converging evidence indicates that hippocampal mRNA translation, required for memory consolidation, is defective in AD. Eukaryotic initiation factor 4E (eIF4E)‐binding protein 2 (4E‐BP2) and Fragile X mental retardation protein (FMRP) act as translational brakes at different stages of protein synthesis. While 4E‐BP2 represses protein synthesis at the initiation step through inhibition of ribosome‐mRNA complex formation, FMRP blocks translation at the mRNA elongation step through ribosome stalling