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- W2045883616 endingPage "1503" @default.
- W2045883616 startingPage "1484" @default.
- W2045883616 abstract "The glutamate neurotransmitter system is one of the major candidate pathways for the pathophysiology of schizophrenia, and increased understanding of the pharmacology, molecular biology and biochemistry of this system may lead to novel treatments. Glutamatergic hypofunction, particularly at the NMDA receptor, has been hypothesized to underlie many of the symptoms of schizophrenia, including psychosis, negative symptoms and cognitive impairment. This review will focus on d-serine, a co-agonist at the NMDA receptor that in combination with glutamate, is required for full activation of this ion channel receptor. Evidence implicating d-serine, NMDA receptors and related molecules, such as d-amino acid oxidase (DAO), G72 and serine racemase (SRR), in the etiology or pathophysiology of schizophrenia is discussed, including knowledge gained from mouse models with altered d-serine pathway genes and from preliminary clinical trials with d-serine itself or compounds modulating the d-serine pathway. Abnormalities in d-serine availability may underlie glutamatergic dysfunction in schizophrenia, and the development of new treatments acting through the d-serine pathway may significantly improve outcomes for many schizophrenia patients. This article is part of a Special Issue entitled ‘Schizophrenia’." @default.
- W2045883616 created "2016-06-24" @default.
- W2045883616 creator A5021367203 @default.
- W2045883616 creator A5075398066 @default.
- W2045883616 creator A5078501123 @default.
- W2045883616 date "2012-03-01" @default.
- W2045883616 modified "2023-10-18" @default.
- W2045883616 title "Contributions of the d-serine pathway to schizophrenia" @default.
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