Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis

Nat Rev Neurosci. 2016 Feb;17(2):125-34. doi: 10.1038/nrn.2015.19. Epub 2016 Jan 14.

Abstract

Molecular, genetic and pathological evidence suggests that deficits in GABAergic parvalbumin-positive interneurons contribute to schizophrenia pathophysiology through alterations in the brain's excitation-inhibition balance that result in impaired behaviour and cognition. Although the factors that trigger these deficits are diverse, there is increasing evidence that they converge on a common pathological hub that involves NMDA receptor hypofunction and oxidative stress. These factors have been separately linked to schizophrenia pathogenesis, but evidence now suggests that they are mechanistically interdependent and contribute to a common schizophrenia-associated pathology.

Publication types

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

MeSH terms

  • Animals
  • Brain / metabolism*
  • Brain / pathology
  • Humans
  • Oxidative Stress / physiology*
  • Receptors, N-Methyl-D-Aspartate / genetics
  • Receptors, N-Methyl-D-Aspartate / metabolism*
  • Schizophrenia / genetics
  • Schizophrenia / pathology*
  • Schizophrenia / physiopathology*

Substances

  • Receptors, N-Methyl-D-Aspartate