News Release

New genetic association with schizophrenia found by researchers

Peer-Reviewed Publication

Elsevier

Philadelphia, PA, February 28, 2008 – Schizophrenia emerges from an altered pattern of brain development, and researchers continue to search for the genes that cause the brain to develop along a path that ultimately leads to schizophrenia. In a high priority article to be published in Biological Psychiatry on March 1st, researchers report their findings on a new genetic link to schizophrenia.

A prior genetic mapping study indicated that a particular gene, multiple epidermal growth factor-like domains 10 or MEGF10, may be associated with schizophrenia. In this new paper, Chen and colleagues directly studied this particular MEGF10 gene in both schizophrenia patients and healthy control subjects. They found that a variant of the MEGF10 gene is associated with the heritable risk for schizophrenia in family-based and case-control genetic studies. Further, the MEGF10 gene appears to be expressed to a greater extent in post-mortem brain tissue from individuals diagnosed with schizophrenia compared to tissue from a group of unaffected individuals.

Dr. Xiangning Chen, corresponding author for this article and assistant professor of psychiatry and human genetics in the Virginia Commonwealth University School of Medicine, explains that “the significance of the paper is that it provides evidence that a gene, i.e. MEGF10, directly involved in apoptosis is found associated with schizophrenia. It has long been speculated that dysfunction of apoptosis may be a cause of schizophrenia, but there [has been] little direct evidence.” Apoptosis is an important biological process of programmed cell death in humans and other complex organisms, and abnormal apoptotic processes have been implicated in a variety of diseases.

John H. Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University School of Medicine and the VA Connecticut Healthcare System, comments on the curiosity of the association between schizophrenia and the MEGF10 gene, which influences the development of skin cells (the epidermis): “One clue may be that nerve cells and skin cells are derived from the same type of primitive cells early in the development of the embryo. Another link may be that features of epidermal development, such as the development of fingerprints, are abnormal in schizophrenia.“

The findings of this study indicate that it may be important for the field of schizophrenia research to more intensively study MEGF10, to understand how it influences brain development, and how it might be related to the treatment of schizophrenia.

###

Notes to Editors:

The article is “MEGF10 Association with Schizophrenia” by Xiangning Chen, Xu Wang, Qi Chen, Vernell Williamson, Edwin van den Oord, Brion S. Maher, F. Anthony O'Neill, Dermot Walsh and Kenneth S. Kendler. Drs. X. Chen, Wang, Q. Chen, Williamson, Maher and Kendler are affiliated with the Department of Psychiatry and Virginia Institute for Psychiatric and Behavior Genetics, Virginia Commonwealth University, Richmond, Virginia. Dr. van den Oord is from the Department of Pharmacy and Center for Biomarker Research and Personalized Medicine, Virginia Commonwealth University, Richmond, Virginia. Dr. O’Neill is with the Department of Psychiatry, The Queens University, Belfast, Northern Ireland. Dr. Walsh is affiliated with The Health Research Board, Dublin, Ireland. The article appears in Biological Psychiatry, Volume 63, Issue 5 (March 1, 2008), published by Elsevier.

Full text of the article mentioned above is available upon request. Contact Jayne M. Dawkins at (215) 239-3674 or ja.dawkins@elsevier.com to obtain a copy or to schedule an interview.

About Biological Psychiatry

This international rapid-publication journal is the official journal of the Society of Biological Psychiatry. It covers a broad range of topics in psychiatric neuroscience and therapeutics. Both basic and clinical contributions are encouraged from all disciplines and research areas relevant to the pathophysiology and treatment of major neuropsychiatric disorders. Full-length and Brief Reports of novel results, Commentaries, Case Studies of unusual significance, and Correspondence and Comments judged to be of high impact to the field are published, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Concise Reviews and Editorials that focus on topics of current research and interest are also published rapidly.

Biological Psychiatry (www.sobp.org/journal) is ranked 4th out of the 95 Psychiatry titles and 16th out of 199 Neurosciences titles on the 2006 ISI Journal Citations Reports® published by Thomson Scientific.

About Elsevier

Elsevier is a world-leading publisher of scientific, technical and medical information products and services. Working in partnership with the global science and health communities, Elsevier's 7,000 employees in over 70 offices worldwide publish more than 2,000 journals and 1,900 new books per year, in addition to offering a suite of innovative electronic products, such as ScienceDirect (http://www.sciencedirect.com/), MD Consult (http://www.mdconsult.com/), Scopus (http://www.info.scopus.com/), bibliographic databases, and online reference works.

Elsevier (http://www.elsevier.com/) is a global business headquartered in Amsterdam, The Netherlands and has offices worldwide. Elsevier is part of Reed Elsevier Group plc (http://www.reedelsevier.com/), a world-leading publisher and information provider. Operating in the science and medical, legal, education and business-to-business sectors, Reed Elsevier provides high-quality and flexible information solutions to users, with increasing emphasis on the Internet as a means of delivery. Reed Elsevier's ticker symbols are REN (Euronext Amsterdam), REL (London Stock Exchange), RUK and ENL (New York Stock Exchange).


Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.