Abstract
The Dopamine Hypothesis has been the leading theory used to explain the mechanism of the clinical manifestation of schizophrenia symptoms for decades. It is unclear if excess dopaminergic activity is the primary pathophysiology causing psychosis or if this dopamine excess is triggered by upstream, downstream or neurodevelopmental abnormalities. A corollary hypothesis suggests that the glutamatergic system may be involved in the pathogenesis of schizophrenia, and that dysfunction of the glutamate system may actually lead to dopamine excess. The NMDA Receptor Hypofunction Hypothesis suggests that malfunctioning NMDA receptors may be the cause for the theoretically hypofunctioning glutamate system. This paper seeks to describe and discuss the potential underlying genetic vulnerabilities of the NMDA receptor and how aberrant genes coding for this receptor may lead to schizophrenia symptoms.
Keywords: NMDA receptor, schizophrenia, glutamate, genetics, Dopamine Hypothesis, neurodevelopmental abnormalities, ion channel, homeostasis, psychosis, psychiatric symptoms
Current Pharmaceutical Design
Title:Genetic Data Supporting the NMDA Glutamate Receptor Hypothesis for Schizophrenia
Volume: 18 Issue: 12
Author(s): Thomas L. Schwartz, Shilpa Sachdeva, Stephen M. Stahl
Affiliation:
Keywords: NMDA receptor, schizophrenia, glutamate, genetics, Dopamine Hypothesis, neurodevelopmental abnormalities, ion channel, homeostasis, psychosis, psychiatric symptoms
Abstract: The Dopamine Hypothesis has been the leading theory used to explain the mechanism of the clinical manifestation of schizophrenia symptoms for decades. It is unclear if excess dopaminergic activity is the primary pathophysiology causing psychosis or if this dopamine excess is triggered by upstream, downstream or neurodevelopmental abnormalities. A corollary hypothesis suggests that the glutamatergic system may be involved in the pathogenesis of schizophrenia, and that dysfunction of the glutamate system may actually lead to dopamine excess. The NMDA Receptor Hypofunction Hypothesis suggests that malfunctioning NMDA receptors may be the cause for the theoretically hypofunctioning glutamate system. This paper seeks to describe and discuss the potential underlying genetic vulnerabilities of the NMDA receptor and how aberrant genes coding for this receptor may lead to schizophrenia symptoms.
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Cite this article as:
Thomas L. Schwartz, Shilpa Sachdeva, Stephen M. Stahl , Genetic Data Supporting the NMDA Glutamate Receptor Hypothesis for Schizophrenia , Current Pharmaceutical Design 2012; 18 (12) . https://dx.doi.org/10.2174/138161212799958594
DOI https://dx.doi.org/10.2174/138161212799958594 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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