For this discussion, describe the ‘dopamine hypothesis of schizophrenia’. What are the relevant updates to this theory? Please cite a scholarly article that was published in the previous five years.
The following article might help as a starting point as you consider this discussion:
Howes, O.D., & Kapur, S. (2009). The dopamine hypothesis of schizophrenia: Version III – The final common pathway. Schizophrenia Bulletin, 35(3), 549-562. doi: 10.1093/schbul/sbp006
Howes and Kapur (2009) advance that the dopamine hypothesis of schizophrenia has been a constant notion in psychiatry. At first, there was a concentration on hyperdopaminergia in the cause for schizophrenia, explain as the version I of etiology. Later it was modified to subcortical hyperdopaminergia along with prefrontal hyperdopaminergia, which is referred to as version II of etiology. Hyperdopaminergia refers to being hyperdopaminergic, which is excessive transmission of dopamine.
Howes and Kapur (2009) explain that these perspectives are too myopic, focusing too much on dopamine, combining psychosis and schizophrenia, and predated biological data.
From the time that version II has been conveyed, there are over 6700 articles about dopamine and schizophrenia have been published. These articles were reviewed in order to make an evaluation of the hypothesis, attending to neurochemical imaging studies, genetic evidence, findings on environmental risks, phenotypes, and animal studies. From this review, Howes and Kapur (2009) suggest a new dopamine hypothesis for schizophrenia that is version III. This hypothesis explores an understanding that includes risk factors such as pregnancy complications, stress and trauma, and genes, which induce dysregulated dopamine. Additionally, there may be brain structural and functional abnormalities that converge to engender neurochemical-induced psychosis that eventually becomes schizophrenia. The main element from this perspective is the implication for treatment. Regarding standard treatment, there is a hyper-focus on the neurotransmitter abnormality. Nevertheless, when it comes to future treatment, there should be greater emphasis on these upstream factors that converge to the eventual dopaminergic dysregulation.
Edwards et al. (2016) advance recent research on the subject, initially pointing out that the dopamine hypothesis, which focuses on the dysregulation of the dopaminergic system, is an ostensible cause for schizophrenia. The research indicates that variation in genes, similar to Howes and Kapur (2009) consideration, is related to dopaminergic functioning which is related to schizophrenia. Edwards et al. (2016) did a meta-analysis of various publicly available datasets. Initially, Edwards et al. (2016) identified a core set of 11 genes, which are involved with dopamine. Thereafter, summary statistics were extracted from those genes related to schizophrenia in order to discover an associated.
The results were that Edwards et al. (2016) did not detect statistically significant outcomes of dopamine-related genes with schizophrenia, but did find genetic signals such as the gene DRD2 locus. This substantiates the conclusion that core genes of the dopaminergic system are not related to the risk of schizophrenia. This does not mean that dopamine does not have a role in schizophrenia; rather it indicates that dopamine-related genes do not substantially affect the genetic risk for schizophrenia. Rather an external variable affects the dysregulation of dopamine which causes schizophrenia.
Edwards, A. C., Bacanu, S. A., Bigdeli, T. B., Moscati, A., & Kendler, K. S. (2016). Evaluating the dopamine hypothesis of schizophrenia in a large-scale genome-wide association study. Schizophrenia research, 176(2-3), 136-140.
Howes, O. D., & Kapur, S. (2009). The dopamine hypothesis of schizophrenia: version IIIthe final common pathway. Schizophrenia bulletin, 35(3), 549-562.