mTOR referees memory and disease through mRNA repression and competition

FEBS Lett. 2017 Jun;591(11):1540-1554. doi: 10.1002/1873-3468.12675. Epub 2017 May 27.


Mammalian target of rapamycin (mTOR) activity is required for memory and is dysregulated in disease. Activation of mTOR promotes protein synthesis; however, new studies are demonstrating that mTOR activity also represses the translation of mRNAs. Almost three decades ago, Kandel and colleagues hypothesised that memory was due to the induction of positive regulators and removal of negative constraints. Are these negative constraints repressed mRNAs that code for proteins that block memory formation? Herein, we will discuss the mRNAs coded by putative memory suppressors, how activation/inactivation of mTOR repress protein expression at the synapse, how mTOR activity regulates RNA binding proteins, mRNA stability, and translation, and what the possible implications of mRNA repression are to memory and neurodegenerative disorders.

Keywords: mRNA; local translation; mammalian target of rapamycin.

Publication types

  • Review

MeSH terms

  • Animals
  • Humans
  • Memory / physiology*
  • Neurodegenerative Diseases / metabolism
  • RNA, Messenger / metabolism*
  • RNA-Binding Proteins / metabolism
  • Synapses / metabolism
  • TOR Serine-Threonine Kinases / metabolism*


  • RNA, Messenger
  • RNA-Binding Proteins
  • TOR Serine-Threonine Kinases