Abstract
Multiple lines of evidence suggest that a dysfunction in the glutamatergic neurotransmission via the N-methyl- D-aspartate (NMDA) receptors contributes to the pathophysiology of psychiatric diseases including schizophrenia. The potentiation of NMDA receptor function may be a useful approach for the treatment of diseases associated with NMDA receptor hypofunction. One possible strategy is to increase synaptic levels of glycine by blocking the glycine transporter-1 (GlyT-1) in glia cells, since glycine acts as a co-agonist site on the NMDA receptor. In this article, the author reviews the recent important patents on GlyT-1 inhibitors for treatment of schizophrenia and other psychiatric diseases associated with the NMDA receptor hypofunction.
Keywords: NMDA receptor, glycine, glycine transporter, glia, cognition, schizophrenia
Recent Patents on CNS Drug Discovery (Discontinued)
Title: Glycine Transporter Inhibitors as Therapeutic Agents for Schizophrenia
Volume: 1 Issue: 1
Author(s): Kenji Hashimoto
Affiliation:
Keywords: NMDA receptor, glycine, glycine transporter, glia, cognition, schizophrenia
Abstract: Multiple lines of evidence suggest that a dysfunction in the glutamatergic neurotransmission via the N-methyl- D-aspartate (NMDA) receptors contributes to the pathophysiology of psychiatric diseases including schizophrenia. The potentiation of NMDA receptor function may be a useful approach for the treatment of diseases associated with NMDA receptor hypofunction. One possible strategy is to increase synaptic levels of glycine by blocking the glycine transporter-1 (GlyT-1) in glia cells, since glycine acts as a co-agonist site on the NMDA receptor. In this article, the author reviews the recent important patents on GlyT-1 inhibitors for treatment of schizophrenia and other psychiatric diseases associated with the NMDA receptor hypofunction.
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Cite this article as:
Hashimoto Kenji, Glycine Transporter Inhibitors as Therapeutic Agents for Schizophrenia, Recent Patents on CNS Drug Discovery (Discontinued) 2006; 1 (1) . https://dx.doi.org/10.2174/157488906775245336
DOI https://dx.doi.org/10.2174/157488906775245336 |
Print ISSN 1574-8898 |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3954 |
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