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The Journal of Neuroscience, October 14, 2009, 29(41):12768-12775; doi:10.1523/JNEUROSCI.3355-09.2009

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Symposia and Mini-Symposia
Understanding the Role of DISC1 in Psychiatric Disease and during Normal Development

Nicholas J. Brandon,1 J. Kirsty Millar,2 Carsten Korth,3 Hazel Sive,4,5,6 Karun K. Singh,7 and Akira Sawa8,9,10

1Discovery Neuroscience, Wyeth Research CN 8000, Princeton, New Jersey 08543, 2Medical Genetics Section, University of Edinburgh Centre for Molecular Medicine and The Institute of Genetics & Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU, United Kingdom, 3Department of Neuropathology, University of Duesseldorf Medical School, 40225 Duesseldorf, Germany, 4Whitehead Institute for Biomedical Research, 5Massachusetts Institute of Technology, and 6Stanley Center for Psychiatric Research, Broad Institute, Cambridge, Massachusetts 02142, 7Picower Institute of Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, and 8Departments of Psychiatry and Behavioral Sciences and 9Neuroscience and 10Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

Correspondence should be addressed to Nicholas J. Brandon at the above address. Email: brandon{at}wyeth.com

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.

Received July 13, 2009; accepted Aug. 7, 2009.

Correspondence should be addressed to Nicholas J. Brandon at the above address. Email: brandon{at}wyeth.com






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