The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
The Role of Genes, Stress, and Dopamine in the Development of Schizophrenia
Open accessAbstract
The dopamine hypothesis is the longest standing pathoaetiological theory of schizophrenia. As it was initially based on indirect evidence and findings in patients with established schizophrenia it was unclear what role dopamine played in the onset of the disorder. However, recent studies in people at risk of schizophrenia have found elevated striatal dopamine synthesis capacity, and increased dopamine release to stress. Furthermore, striatal dopamine changes have been linked to altered cortical function during cognitive tasks, in-line with preclinical evidence that a circuit involving cortical projections to the striatum and midbrain may underlie the striatal dopamine changes. Other studies have shown that a number of environmental risk factors for schizophrenia, such as social isolation and childhood trauma, also impact on presynaptic dopaminergic function. Advances in preclinical work and genetics have begun to unravel the molecular architecture linking dopamine, psychosis and psychosocial stress. Included among the many genes associated with risk of schizophrenia, are the gene encoding the DRD2 receptor and those involved in the up-stream regulation of dopaminergic synthesis, through glutamatergic and gamma-aminobutyric acid (GABA)-ergic pathways. A number of these pathways are also linked to the stress response. We review these new lines of evidence and present a model of how genes and environmental factors may sensitise the dopamine system so that it is vulnerable to acute stress, leading to progressive dysregulation and the onset of psychosis. Finally, we consider the implications for rational drug development, in particular regionally selective dopaminergic modulation, and the potential of genetic factors to stratify patients.
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Cites
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Cited by
Dopamine: Functions, Signaling, and Association with Neurological Diseases
Klein, M. O., Battagello, D. S., Cardoso, A. R., Hauser, D. N., Bittencourt, J. C., & Correa, R. G. (2019) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-018-0632-3 · Cited by 1,073
McCutcheon, R., Beck, K., Jauhar, S., & Howes, O. D. (2018) · Schizophrenia Bulletin · doi:10.1093/schbul/sbx180 · Cited by 305
Self-citationThe Role of Estrogen in Brain and Cognitive Aging
Russell, J. K., Jones, C. K., & Newhouse, P. A. (2019) · Neurotherapeutics · doi:10.1007/s13311-019-00766-9 · Cited by 257
Onwordi, E. C., Halff, E. F., Whitehurst, T., Mansur, A., Cotel, M.-C., Wells, L., Creeney, H., Bonsall, D., Rogdaki, M., Shatalina, E., et al. (2020) · Nature Communications · doi:10.1038/s41467-019-14122-0 · Cited by 243
Self-citationJauhar, S., Nour, M. M., Veronese, M., Rogdaki, M., Bonoldi, I., Azis, M., Turkheimer, F., McGuire, P., Young, A. H., & Howes, O. D. (2017) · JAMA Psychiatry · doi:10.1001/jamapsychiatry.2017.2943 · Cited by 233
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Metadata
- Authors
- Howes, O. D., McCutcheon, R., Owen, M. J., & Murray, R. M.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2017-01
- Volume
- 81
- Issue
- 1
- Pages
- 9-20
- ISSN
- 0006-3223 (ISSN-L)
- OpenAlex
- W2486451269
- Cited by
- 601
- References
- 44
- FWCI
- 46.31
- Type
- journal article
- Language
- en
- Open access
- green
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