title: Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis.
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.
authors.affiliation: School of Biomedical Sciences, University of Edinburgh, George Square, Edinburgh EH8 9XD, UK.
authors.forename: Giles E
authors.initials: GE
authors.lastname: Hardingham
authors.affiliation: Department of Psychiatry, Center of Psychiatric Neuroscience, Centre Hospitalier Universitaire Vaudois and University of Lausanne, CH-1008, Prilly-Lausanne, Switzerland.
authors.forename: Kim Q
authors.initials: KQ
authors.lastname: Do
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D018384:Oxidative Stress / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics / Q000378:metabolism*; D012559:Schizophrenia / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology*
chemical_list: D016194:Receptors, N-Methyl-D-Aspartate