Linking early-life NMDAR hypofunction and oxidative stress inyschizophrenia pathogenesis

Research output: Contribution to journalLiterature reviewpeer-review

Abstract / Description of output

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 inter-dependent and contribute to a common schizophrenia-associated pathology.

Original languageEnglish
Pages (from-to)1-9
Number of pages9
JournalNature Reviews Neuroscience
Volume17
Issue number2
DOIs
Publication statusPublished - 14 Jan 2016

Keywords / Materials (for Non-textual outputs)

  • N-ACETYL-CYSTEINE
  • INTRINSIC ANTIOXIDANT DEFENSES
  • GLUTATHIONE-DEFICIENT MICE
  • AUTISM SPECTRUM DISORDERS
  • CEREBROSPINAL-FLUID
  • PREFRONTAL CORTEX
  • DOUBLE-BLIND
  • MOUSE MODEL
  • D-SERINE
  • PARVALBUMIN INTERNEURONS

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