Glutamate hypothesis in schizophrenia

Schizophrenia is a chronic and severe psychiatric disorder that has profound impact on an individual’s life and on society. Thus, developing more effective therapeutic interventions is essential. Over the past quarter‐century, an abundance of evidence from pharmacologic challenges, post‐mortem studi...

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Vydané v:Psychiatry and clinical neurosciences Ročník 73; číslo 5; s. 204 - 215
Hlavní autori: Uno, Yota, Coyle, Joseph T.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Melbourne John Wiley & Sons Australia, Ltd 01.05.2019
Wiley Subscription Services, Inc
Predmet:
Clinical trials
D‐serine
glutamate
Glutamatergic transmission
Glutamic acid receptors
Mental disorders
N-Methyl-D-aspartic acid receptors
Neuroimaging
Neurotransmission
N‐methyl‐d‐aspartate receptor
Schizophrenia
serine racemase
Therapeutic applications
serine racemase
D-serine
schizophrenia
N-methyl-d-aspartate receptor
glutamate
ISSN:1323-1316, 1440-1819, 1440-1819
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Abstract Schizophrenia is a chronic and severe psychiatric disorder that has profound impact on an individual’s life and on society. Thus, developing more effective therapeutic interventions is essential. Over the past quarter‐century, an abundance of evidence from pharmacologic challenges, post‐mortem studies, brain imaging, and genetic studies supports the role of glutamatergic dysregulation in the pathophysiology of schizophrenia, and the results of recent randomized clinical trials based on this evidence have yielded promising results. In this article, we review the evidence that alterations in glutamatergic neurotransmission, especially focusing on the N‐methyl‐d‐aspartate receptor (NMDAR) function, may be a critical causative feature of schizophrenia, how this contributes to pathologic circuit function in the brain, and how these insights are revealing whole new avenues for treatment development that could reduce treatment‐resistant symptoms, which account for persistent disability.
AbstractList Schizophrenia is a chronic and severe psychiatric disorder that has profound impact on an individual’s life and on society. Thus, developing more effective therapeutic interventions is essential. Over the past quarter‐century, an abundance of evidence from pharmacologic challenges, post‐mortem studies, brain imaging, and genetic studies supports the role of glutamatergic dysregulation in the pathophysiology of schizophrenia, and the results of recent randomized clinical trials based on this evidence have yielded promising results. In this article, we review the evidence that alterations in glutamatergic neurotransmission, especially focusing on the N‐methyl‐d‐aspartate receptor (NMDAR) function, may be a critical causative feature of schizophrenia, how this contributes to pathologic circuit function in the brain, and how these insights are revealing whole new avenues for treatment development that could reduce treatment‐resistant symptoms, which account for persistent disability.
Schizophrenia is a chronic and severe psychiatric disorder that has profound impact on an individual's life and on society. Thus, developing more effective therapeutic interventions is essential. Over the past quarter-century, an abundance of evidence from pharmacologic challenges, post-mortem studies, brain imaging, and genetic studies supports the role of glutamatergic dysregulation in the pathophysiology of schizophrenia, and the results of recent randomized clinical trials based on this evidence have yielded promising results. In this article, we review the evidence that alterations in glutamatergic neurotransmission, especially focusing on the N-methyl-d-aspartate receptor (NMDAR) function, may be a critical causative feature of schizophrenia, how this contributes to pathologic circuit function in the brain, and how these insights are revealing whole new avenues for treatment development that could reduce treatment-resistant symptoms, which account for persistent disability.Schizophrenia is a chronic and severe psychiatric disorder that has profound impact on an individual's life and on society. Thus, developing more effective therapeutic interventions is essential. Over the past quarter-century, an abundance of evidence from pharmacologic challenges, post-mortem studies, brain imaging, and genetic studies supports the role of glutamatergic dysregulation in the pathophysiology of schizophrenia, and the results of recent randomized clinical trials based on this evidence have yielded promising results. In this article, we review the evidence that alterations in glutamatergic neurotransmission, especially focusing on the N-methyl-d-aspartate receptor (NMDAR) function, may be a critical causative feature of schizophrenia, how this contributes to pathologic circuit function in the brain, and how these insights are revealing whole new avenues for treatment development that could reduce treatment-resistant symptoms, which account for persistent disability.
Schizophrenia is a chronic and severe psychiatric disorder that has profound impact on an individual’s life and on society. Thus, developing more effective therapeutic interventions is essential. Over the past quarter‐century, an abundance of evidence from pharmacologic challenges, post‐mortem studies, brain imaging, and genetic studies supports the role of glutamatergic dysregulation in the pathophysiology of schizophrenia, and the results of recent randomized clinical trials based on this evidence have yielded promising results. In this article, we review the evidence that alterations in glutamatergic neurotransmission, especially focusing on the N ‐methyl‐ d ‐aspartate receptor (NMDAR) function, may be a critical causative feature of schizophrenia, how this contributes to pathologic circuit function in the brain, and how these insights are revealing whole new avenues for treatment development that could reduce treatment‐resistant symptoms, which account for persistent disability.
Author Coyle, Joseph T.
Uno, Yota
Author_xml – sequence: 1
  givenname: Yota
  surname: Uno
  fullname: Uno, Yota
  email: yota_u@ypdc.net
  organization: University of Bath
– sequence: 2
  givenname: Joseph T.
  surname: Coyle
  fullname: Coyle, Joseph T.
  organization: McLean Hospital
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30666759$$D View this record in MEDLINE/PubMed
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Keywords serine racemase
D-serine
schizophrenia
N-methyl-d-aspartate receptor
glutamate
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Snippet Schizophrenia is a chronic and severe psychiatric disorder that has profound impact on an individual’s life and on society. Thus, developing more effective...
Schizophrenia is a chronic and severe psychiatric disorder that has profound impact on an individual's life and on society. Thus, developing more effective...
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SubjectTerms Clinical trials
D‐serine
glutamate
Glutamatergic transmission
Glutamic acid receptors
Mental disorders
N-Methyl-D-aspartic acid receptors
Neuroimaging
Neurotransmission
N‐methyl‐d‐aspartate receptor
Schizophrenia
serine racemase
Therapeutic applications
Title Glutamate hypothesis in schizophrenia
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fpcn.12823
https://www.ncbi.nlm.nih.gov/pubmed/30666759
https://www.proquest.com/docview/2218074341
https://www.proquest.com/docview/2179403059
Volume 73
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