[Curing mental retardation: searching for balance]

Med Sci (Paris). 2011 Jan;27(1):70-6. doi: 10.1051/medsci/201127170.
[Article in French]

Abstract

Mental retardation (MR) occurs in 2 to 3 % of the general population and is still not therapeutically addressed. Milder forms of MR result from deficient synaptogenesis and/or impaired synaptic plasticity during childhood. These alterations would result from disequilibrium in signalling pathways regulating the balance between long term potentiation (LTP) and long term depression (LTD) in certain neurons such as hippocampus neurons. To provide mentally retarded children with increased cognitive abilities, novel experimental approaches are currently being developed to characterize signalling status associated with MR and to identify therapeutic targets that would restore lost equilibrium. Several studies also highlighted the major role played by molecular switches like kinases, phosphatases, small G proteins and their regulators in the coordination and integration of signalling pathways associated with synaptic plasticity. These proteins may therefore constitute promising therapeutic targets for a number of cognitive deficiencies.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / physiology
  • Cognition / physiology
  • Dendrites / ultrastructure
  • Disease Models, Animal
  • Drug Design
  • GTP Phosphohydrolases / physiology
  • Hippocampus / pathology
  • Humans
  • Intellectual Disability / drug therapy*
  • Intellectual Disability / epidemiology
  • Intellectual Disability / pathology
  • Intellectual Disability / physiopathology
  • Models, Neurological
  • Multigene Family
  • Nerve Tissue Proteins / physiology
  • Neuronal Plasticity / drug effects
  • Neuronal Plasticity / physiology
  • Nootropic Agents / pharmacology
  • Nootropic Agents / therapeutic use*
  • Phosphoprotein Phosphatases / physiology
  • Phosphorylation / drug effects
  • Protein Kinases / physiology
  • Protein Processing, Post-Translational / drug effects
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • Synaptic Transmission / drug effects
  • Synaptic Transmission / physiology

Substances

  • Nerve Tissue Proteins
  • Nootropic Agents
  • Protein Kinases
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • Phosphoprotein Phosphatases
  • GTP Phosphohydrolases