Understanding the Role of DISC1 in Psychiatric Disease and during Normal Development
Open accessAbstract
The biology of schizophrenia is complex with multiple hypotheses (dopamine, glutamate, neurodevelopmental) well supported to underlie the disease. Pathways centered on the risk factor “disrupted in schizophrenia 1” (DISC1) may be able to explain and unite these disparate hypotheses and will be the topic of this mini-symposium preview. Nearly a decade after its original identification at the center of a translocation breakpoint in a large Scottish family that was associated with major psychiatric disease, we are starting to obtain credible insights into its function and role in disease etiology. This preview will highlight a number of exciting areas of current DISC1 research that are revealing roles for DISC1 during normal brain development and also in the disease state. Together these different threads will provide a timely and exciting overview of the DISC1 field and its potential in furthering our understanding of psychiatric diseases and in developing new therapies.
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Current models of schizophrenia suggest that the disorder is due to both common and rare gene mutations, copy-number variations, and possibly epigenetic factors, all of which can affect multiple brain neurotransmitter systems and multiple risk genes.
“Current models of schizophrenia suggest that the disorder is due to both common and rare gene mutations, copy-number variations, and possibly epigenetic factors [361], all of which can affect multiple brain neurotransmitter systems and multiple risk genes [362-364].”
From Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings (2012) · cites this paper as [363]
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References 52 · Cited by 198
Research works printed but not linked: 1
- Blaker A, DeRienzo G, Sive H (2009) Zebrafish as a tool to study autism. In: Autism spectrum disorders (Amaral DG, Dawson G, Geschwind DH, eds), in press. Oxford: Oxford UP.
- Authors
- Brandon, N. J., Millar, J. K., Korth, C., Sive, H., Singh, K. K., & Sawa, A.
- Affiliations
- Wyeth (US)
- University of Edinburgh (GB)
- Heinrich Heine University Düsseldorf (DE)
- Broad Institute (US)
- Massachusetts Institute of Technology (US)
- Johns Hopkins University (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2009-10-14
- Volume
- 29
- Issue
- 41
- Pages
- 12768-12775
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6665304
- OpenAlex
- W2053045480
- Cited by
- 198
- References
- 52
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 4 · 2023: 1 · 2022: 12 · 2021: 5 · 2020: 6 · 2019: 6 · 2018: 7 · 2017: 6 · 2016: 17 · 2015: 9 · 2014: 11 · 2013: 16 · 2012: 21
- FWCI
- 3.61
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Social Sciences › Arts and Humanities › Philosophy › Mental Health and Psychiatry
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- DISC1, schizophrenia, mental illness, brain development, neurodevelopmental hypothesis, dopamine hypothesis, glutamate hypothesis, translocation breakpoints, etiology, therapeutic target
- MeSH terms
- Animals, Mental Disorders, Brain, Disease Models, Animal, Humans, Models, Biological, Nerve Tissue Proteins, Risk Factors, Synapses, Signal Transduction, Gene Expression Regulation, Developmental, Genetic Predisposition to Disease
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