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 inter-dependent and contribute to a common schizophrenia-associated pathology.
Original language | English |
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Pages (from-to) | 1-9 |
Number of pages | 9 |
Journal | Nature Reviews Neuroscience |
Volume | 17 |
Issue number | 2 |
DOIs | |
Publication status | Published - 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