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Archive - Sep 21, 2011


Genetic Overlap Found Between Schizophrenia and Bipolar Disorder

Knowledge about the biological origin of diseases like schizophrenia, bipolar disorder, and other psychiatric conditions is critical to improving diagnosis and treatment. In an effort to push the field forward, three UCLA researchers, along with scientists from more than 20 countries, have been taking part in one of the largest collaborative efforts in psychiatry — a genome-wide study involving more than 50,000 study participants aimed at identifying which genetic variants make people susceptible to psychiatric disease. This collaborative, the Psychiatric Genome-Wide Association Study Consortium (PGC), now reports, in two articles in the September 18, 2011 online edition of Nature Genetics, that it has discovered that common genetic variants contribute to a person's risk of schizophrenia and bipolar disorder. The PGC's studies provide new molecular evidence that 11 regions on the genome are strongly associated with these diseases, including six regions not previously observed. The researchers also found that several of these DNA variations contribute to both diseases. The findings, the researchers say, represent a significant advance in understanding the causes of these chronic, severe, and debilitating disorders. The UCLA researchers who contributed to the schizophrenia study are Dr. Roel A. Ophoff, a professor of psychiatry and human genetics and one of the founding principal investigators of the schizophrenia portion of the study; Dr. Nelson Freimer, a professor of psychiatry and director of the Center for Neurobehavioral Genetics at the Semel Institute for Neuroscience and Human Behavior at UCLA; and Dr. Rita Cantor, a professor of psychiatry and human genetics. Schizophrenia and bipolar disorder are common and often devastating brain disorders.

Identificatioon of Key Molecule That Blocks Angiogenesis in Tumors

A new and better understanding of blood vessel growth and vascular development (angiogenesis) in cancer has been made possible by research carried out by a team of scientists from the Moffitt Cancer Center, the University of Florida, Harvard University, Yale University, and the Children's Hospital of Los Angeles. The research team published the results of its investigation in the September 13, 2011 issue of the Proceedings of the National Academy of Sciences. "Vascular development is a fundamental biological process that is tightly controlled by both pro-and anti-angiogenic mechanisms," said Dr. Edward Seto, a co-author of the study and professor and chairman of the Department of Molecular Oncology at Moffitt. "Physiological angiogenesis occurs in adults only under specific settings. Excess angiogenesis contributes to a variety of diseases, including cancer. In cancer, vascular endothelial growth factor (VEGF) is commonly overproduced." The goal of the research was to determine how angiogenesis is regulated by positive and negative biological activities. "Understanding the biological principles that direct vascular growth has important clinical implications because cancers are highly vascularized," concluded Dr. Seto. This meant seeking a better understanding of the relationship between the chromatin insulator binding factor CTCF and how it regulates VEGF expression. "At the heart of vascular development is VEGF which, in precise doses, is an important stimulator of normal blood vessel growth," explained Dr. Seto. "However, VEGF - probably the most important stimulator of normal and pathological blood vessel growth - is regulated by a number of factors." According to Dr. Seto, the study suggests that CTCF can block VEGF from being activated.